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C681  .N79  Studies  in  cardiac  p 


RECAP 


Columbia  ©nibersiitp 
intftcCitpofJ^etD^orb 

COLLEGE  OF  PHYSICIANS 
AND   SURGEONS 


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STUDIES 


Cardiac  Pathology 


GEORGE  WILLIAM  NORRIS,  A.B.,  M.D. 

ASSOCIATE    IN    MEDICINE    AT    THE    UNIVERSITY   OF   PENNSYLVANIA 

VISITING     PHYSICIAN    TO    THE     EPISCOPAL    HOSPITAL    OF    PHILADELPHIA 

ASSISTANT   VISITING    PHYSICIAN   TO  THE    UNIVERSITY   AND  TO   THE    PHILADELPHIA  GENERAL    HOSPITALS 

PHYSICIAN    TO  THE   MEDICAL   OUT-PATIENT    DEPARTMENT  OF   THE    PENNSYLVANIA    HOSPITAL 

FELLOW    OF   THE  COLLEGE    OF    PHYSICIANS   OF   PHILADELPHIA.    ETC. 


WITH  8s  ORIGINAL  ILLUSTRATIONS 


PHILADELPHIA   AND    LONDON 

W.    B.   SAUNDERS   COMPANY 

1911 


Copyright,  1911,  by  W.  B.  Saunders  Company 


PRINTED   IN  AMERICA 


TO 

THE    MEMORY    OF   MY    GRANDFATHER 

GEORGE  W.  NORRIS 

CLINICAL   PROFESSOR   OF   SURGERY   AT   THE    UNIVERSITY   OF   PENNSYLVANIA 
AND    OF   MY    FATHER 

WILLIAM  FISHER  NORRIS 

PROFESSOR   OF   OPHTHALMOLOGY   AT   THE    UNIVERSITY   OF   PENNSYLVANIA 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/studiesincardiacOOnorr 


PREFACE 


The  opportunity  of  photographing  specimens  in  the  museums 
of  five  of  the  most  important  hospitals  of  Philadelphia  having  been 
afforded  the  author  through  the  courtesy  of  the  respective  patholo- 
gists of  those  institutions,*  it  has  seemed  worth  while  to  reproduce 
the  same  in  order  to  secure  for  these  interesting  examples  of  cardiac 
pathology  a  more  enduring  permanence  and  a  more  widespread 
field  of  usefulness.  In  order  to  enhance  the  value  of  the  exhibit 
considerable  data  bearing  on  the  pathology  of  cardiac  lesions 
have  been  added.  No  attempt  has  been  made  to  publish  a  com- 
plete work  on  the  pathology  of  the  heart,  the  text  being  mainh'  in 
the  form  of  an  explanation  and  an  elucidation  of  the  illustrations, 
and  but  little  space  has  been  devoted  to  the  microscopic  tissue 
changes.  The  result  is  perhaps  open  to  criticism  as  being  too 
statistical  in  nature,  and  the  same  set  of  statistics  can,  as  we  know, 
only  too  often,  be  manipulated  to  prove  opposing  hypotheses.  On 
the  other  hand,  it  cannot  be  denied  that  statistic  compilation  has 
done  considerable  for  the  advance  of  medical  science,  and  there  is 
much  truth  in  Kant's  dictum  that  the  amount  of  pure  science  which 
any  given  study  contains  is  in  direct  proportion  to  the  quantity  of 
mathematics  it  includes. 

The  author  has  endeavored  to  give  due  credit  to  all  concerned, 

*  The  author  desires  to  express  his  indebtedness  to  the  following  gentlemen  for  their 
courtesy  in  placing  the  pathologic  material  of  the  various  institutions  with  which  they  are  con- 
nected at  his  disposal:  Professor  Allen  J.  Smith  of  the  University  of  Pennsylvania,  Dr.  A.  O.  J. 
Kelly  of  the  German  Hospital,  Dr.  W.  T.  Longcope  of  the  Pennsylvania  Hospital,  Dr.  R.  C. 
Rosenberger  of  the  Philadelphia  General  Hospital,  Dr.  C.  Y.  White  of  the  Protestant  Epis- 
copal Hospital,  Dr.  George  Fetterolf  and  Dr.  Alfred  R.  Allen  of  the  University  of  Pennsyl- 
vania, and  Dr.  George  McClellan  of  the  College  of  Physicians  of  Philadelphia. 


not  only  in  the  matter  of  specimens  but  also  in  regard  to  the 
sources  of  information.  This  has  added  very  greatly  to  the  time 
consumed  in  the  preparation  of  the  work  and  it  is  hoped  that  the 
attempt  has  been  sufficiently  successful  to  do  justice  to  the  authori- 
ties quoted  and  to  assist  such  readers  as  may  be  desirous  of  more 
detailed  information. 

George  W.  Norris. 

1530  Locust  Street, 

Philadelphia,  March,  1911. 


CONTENTS 


PAGE 

Acute  Endocarditis 1 

Chronic  Infective  Endocarditis 30 

Chronic  Endocarditis 39 

Diseases  of  the  Aortic  Orifice 50 

Aortic  Obstruction 50 

Aortic  Insufficiency 55 

Diseases  of  the  Mitral  Orifice 64 

Mitral  Obstruction 64 

Mitral  Insufficiency 80 

Diseases  of  the  Tricuspid  Orifice 86 

Tricuspid  Obstruction 87 

Tricuspid  Insufficiency 92 

Diseases  of  the  Pulmonary  Orifice 96 

Pulmonary  Obstruction 96 

Pulmonary  Insufficiency 98 

Acute  Pericarditis 100 

Chronic  Pericarditis 124 

Cardiac  Hypertrophy 136 

Cardiac  Dilatation ' 162 

Coronary  Arteriosclerosis 180 

Cardiac  Aneurism 188 

Cardiac  Thrombosis 192 

Tumors  of  the  Heart 198 

Cardiac  Syphilis 200 

Congenital  Lesions 206 

Imperforate  Ventricular  Septum 206 

Transposition  of  the  Great  Vessels 212 

Patulous  Ductus  Arteriosus 212 

Patulous  Foramen  Ovale 214 

Anomalies  of  the  Semilunar  Valves 219 

Double  Mitral  or  Tricuspid  Orifices 219 

Index  of  Illustrations 229 

Index  of  Subjects  231 


STUDIES    IN 
CARDIAC    PATHOLOGY 


I.  ACUTE  ENDOCARDITIS 

Experimental  evidence  indicates  that  for  the  production  of 
an  acute  endocarditis  two  factors  are  necessary.  First,  a  pre- 
disposition or  preparation  on  the  part  of  the  endocardium,  which 
may  be  produced  by  mechanical,  chemical,  or  toxic  action;  and, 
second,  the  presence  of  pathogenic  micro-organisms.  There  has 
been  much  debate  as  to  whether  toxemia  alone  can  ever  produce 
verrucose  lesions.  Di  Vecchi  ^  has  done  considerable  work  on 
this  question,  and  believes  that  he  has  been  able  to  produce 
endocarditis  by  the  injection  of  bacterial  toxins  together  with 
mechanically  and  chemically  irritant  substances,  such  as  coal- 
dust  and  argentic  nitrate.  Fulci,  who  has  repeated  the  last- 
mentioned  experiments,  was  unable  to  produce  lesions  which  were 
not  also  found  in  the  control  animals,  unless  living  organisms 
were  also  injected.-  He  found,  however,  that  toxins  and  me- 
chanical irritants  distinctly  helped  in  preparing  the  endocardium 
for  the  inflammatory  process.  These  last  findings  are  quite 
in  accord  with  those  of  other  capable  investigators.  The  mere 
fact  that  we  are  not  always  able  to  demonstrate  organisms  in 
the  valvular  lesions  of  endocarditis  is  to  be  explained,  first,  by 
their  occasional  disappearance  after  the  lesions  have  been  pro- 
duced; second,  by  inadequacy  of  our  methods  of  investigation; 
and,  third,  by  the  fact  that  in  some  instances  we  are  doubtless 

'Arch,  di  Anat.  Putholog.  c  .Sfiierizf,  190.5,  and  ]iullet.  dolhi  ScicnzR  med.  di  Bologna, 
Jan.,  1908. 

2  Fulci:   Bcitr.  ■/..  pa1.li.  Anat,.  u.  ■/,.  allg.  Patli.,  I9(1S,  ]).  :M9. 
1  I 


2  STUDIES  IN  CARDIAC  PATHOLOGY 

dealing  with  the  effects  of  as  j'et  undiscovered  organisms,  such  as 
those  responsible  for  scarlatina,  measles,  chorea,  etc. 

We  are  forced  to  conclude,  therefore,  that  all  cases  of  acute 
verrucose  and  ulcerative  processes  on  the  endocardium  are  in- 
fectious in  origin.  This,  of  course,  does  not  include  purely  sclerotic 
processes,  which  are  probablj-  brought  about  in  a  similar  manner 
to  arteriosclerosis  elsewhere. 

Recent  advances  in  bacteriology  have  tended  to  simplify 
greatly  the  subject  of  infective  endocarditis.  Much  more  accurate 
results  are  obtained  by  means  of  intra-vitam  blood-cultures  than 
by  cultures  from  the  heart's  blood  at  autopsy,  in  which  there  is 
always  a  tendency  for  terminal  infection  to  play  a  role.  This 
fact  probably  explains  the  complex  and  hardly  identifiable  micro- 
organisms described  by  some  early  observers. 


Fig.  1, — Acute  Ulcerative  Mitral  Endocarditis. 

Female,  white,  aged  forty  years.  (Pennsylvania  Hospital.  Autop.sy  408.  Pathologist: 
Dr.  Longcope.     Ph3fsician:  Dr.  M.  J.  Lewis.) 

Clinical  History;  Denies  previous  diseases.  Well  until  two  weeks  ago,  since  which 
time  she  has  had  pain  in  the  left  side  and  a  harassing  nocturnal  cough,  without  expectoration . 
Night-sweats,  dyspnea,  and  edema  of  the  legs,  also  slight  palpitation,  were  present. 

Physical  Examination:  A  loud  vibratory  systolic  murmur  is  heard  over  the  body  of  the 
heart,  which  is  transmitted  to  the  left  scapula,  and  can  be  heard  over  the  whole  chest  and 
abdomen.     A  soft  systolic  murmur  is  noted  at  the  aortic  area. 

Pathologic  Diagnosis:  Acute  ulcerative  mitral  endocarditis.  Thrombosis  of  a  small 
branch  of  the  pulmonary  artery.  Acute  bronchopneumonia.  Anemic  infarction  of  the  spleen 
and  kidneys. 

Heart:  The  heart  weighs  410  grams.  The  vessels  are  injected  and  a  few  punctate 
hemorrhages  are  noted  below  the  serous  surface.  The  cavities  contain  postmortem  clots. 
The  right  ventricle  is  somewhat  dilated.  The  endocardium  is  thickened.  The  mitral  valve  is 
the  seat  of  a  most  extensive  vegetative  growth,  situated  above  the  junction  of  the  anterior  and  posterior 
leaflets.  Beneath  it  the  valve  is  extensively  ulcerated,  and  several  chordce  lendinece  swing  loose,, 
being  attached  only  to  the  vegetations.  The  vegetative  inass  is  lobulated  and  nearly  the  size  of  a 
walnut;  it  extends  to  the  auricular  surface  for  2.5  to  3  cm.,  and  when  the  heart  is  held  in  the  up- 
right position,  "practically  fills  the  auriculo-ventricular  orifice.  The  vegetations  are  delicate,  gray, 
soft,  friable,  and  lobulated.  Numerous  soft,  gray,  pinhead-size  vegetations  cover  the  posterior 
leaflet  and  part  of  the  auricular  wall.  The  aortic  valves  are  thickened  and  somewhat  calcified 
at  the  bases,  but  show  neither  retraction  nor  vegetation.  The  muscle  is  soft,  brownish-gray, 
and  fragments  easily.  The  coronary  arteries  show  an  extensive  grade  of  sclerosis,  and  in 
places  are  converted  into  rigid  tubes.  The  aorta  immediately  above  the  valves,  shows  a  diffuse 
dilatation,  measuring  9  cm.  in  circumference.     Its  wall  is  fairly  smooth. 

Microscopic  Diagnosis:  The  pericardium  is  normal.  Muscle-fibers  are  rather  granular 
and  have  partially  lost  their  cross-strise.  Between  them  some  connective-tissue  formation  is 
noted.  The  valvular  vegetations  showed  diplococci,  slightly  lanceolate  in  form,  Gram-positive. 
Cultures  showed  numerous  very  small  pin-point  colonies,  barely  visible  to  the  naked  eye. 


Fk;.   1. 


4  STUDIES    IN    CARDIAC    PATHOLOGY 

Classification. — A  satisfactoiy  classification  of  acute  infectious 
endocarditis  is  at  present  impossible.  No  distinctions  can  be 
made  which  will  alwaj^s  hold  good.  A  division  into  simple  and 
infective  is  fallacious,  since  ]3robabl}^  all  cases  are  infectious  in 
origin.  Benign  and  malignant  is  equally  unsatisfactor}-,  inasmuch 
as  there  are  no  "benign"  cases,  the  endocardial  changes  instituted 
being  always  sooner  or  later  serious.  A  bacteriologic  classifica- 
tion is  also  objectionable,  because  although  certain  micro-organisms 
tend  on  the  whole  to  produce  certain  tjqDes  of  changes,  yet  there 
are  so  many  exceptions  and  uncertainties  as  to  make  this  basis 
infeasible.  Finally,  a  classification  into  simple,  ulcerative,  ver- 
rucose,  etc.,  based  upon  anatomic  appearances  is  useless,  since 
these  are  not  radical  differences,  but  largely  accidental  charac- 
teristics, which  merge  more  or  less  insensiblj^  into  each  other. 
On  the  other  hand,  there  are  clinical  types  of  the  disease  which 
are  quite  distinct  from  each  other,  in  the  onset,  course,  and  termina- 
tion, so  that  some  sort  of  differentiation  must  be  attempted.     Osier 


Fig.  2. — Malignant  Endocarditis,  Aortic  and  Mitral. 

J.  M.,  male,  white,  aged  thirty-three  years.  (Philadelphia  Hospital.  Autopsy:  Vol. 
xxii,  p.  32.     Phj'sician:   Dr.  J.  Tyson.     Pathologist:   Dr.  Foster.) 

Clinical  Notes':  Laborer,  hard  worker.  Alcohol  to  excess.  Tobacco  moderate;  de- 
nies sj'philis.  Malaria  in  Philippines.  Rheumatism  three  years  ago.  Epigastric  pain,  cough, 
hemoptysis,  vertigo,  diplopia.  Corrigan  pulse;  radial  sclerosis.  Heart  enlarged  to  right  and 
left.  First  sound  only  fair.  Pulmonic  second  accentuated.  Apex-beat:  sixth  interspace, 
1  in.  outside  midclavicular  line.     Systolic  murmur  at  third  left  costal  cartilage. 

Pathologic  Diagnosis:  Malignant  endocarditis — aortic  and  mitral;  aortic  insufficiency; 
parenchymatous  degeneration  of  heart;  hemorrhagic  infarcts  of  kidnej',  spleen;  fatty  de- 
generation of  liver;  chronic  parenchymatous  nephritis,  with  beginning  interstitial  changes; 
healed  bilateral  pulmonary  tuberculosis,  etc. 

Pericardium:  Contains  60  c.c.  of  blood-tinged  fluid.  Serous  surface  smooth  and  glis- 
tening. 

Heart:  Weighs  470  grams;  is  large  and  flabby;  pale  in  color.  Absence  of  epicardial 
fat.  Vessels  prominent  and  engorged.  Aortic  valves  incompeLenl  to  water  lest.  Heart 
muscle  soft,  brownish-red,  and  granular.  Papillary  muscles  pale.  Aortic  orifice,  8;  mitral,  11; 
tricuspid,  14;  pulmonary,  7  cm.  in  circumference. 

On  the  anterior  and  left  -posterior  aortic  leaflets  there  are  rough,  reddish-yellow  vegetations 
about  1  cm.  in  diameter.  On  the  ventricular  surface  of  the  mitral  leaflet  there  is  a  large,  irregidar, 
cauliflower-like  mass,  ii  xS  x  1 .5  cm.  Inflammatory  changes  incident  to  this  massive  vegetation 
have  occurred  on  the  auricular  surface  of  this  leaflet,  and  consist  of  three  circumscribed  areas 
of  roughening  covered  with  plastic  lymph.  The  other  valves  are  uninvolved.  The  base  of 
the  aorta  shows  beginning  atheromatous  change  about  the  coronary  orifices. 


6  STUDIES  IN  CARDIAC  PATHOLOGY 

has  suggested  the  following  division:  (1)  malignant;  (2)  simple 
acute;    (3)  chronic. 

The  virulence  of  the  causative  organism  is  often  more  im- 
portant than  the  species.  Organisms  of  low  virulence  may  produce 
severe  subacute  attacks  without  the  production  of  any  bactericidal 
reaction  on  the  part  of  the  host.  The  main  difference  between 
these  types  is  in  the  amount  of  endocardial  inflammation  and 
tissue  necrosis.  In  malignant  endocarditis  emboli  are  more  fre- 
quent and  more  septic,  right-sided  involvement  more  common, 
and  micro-organisms  are  oftener  found  in  the  blood,  in  the  emboli, 
and  on  the  valves.  These  cases  are  nearly  always  secondary 
and  generally  fatal.  Infants  and  children  seem  to  be  almost 
exempt  from  this  form  of  the  disease.^ 

Morbid  Anatomy. — The  earliest  visible  manifestation  of  acute 
endocarditis  consists  in  an  opaque  or  slightly  rough  area  upon 
the  valves  or  endocardium.  If  the  process  continues,  bead-like, 
nodular  elevations  appear  which  eventually  develop  into  distinct 
verrucse.  The  amount  of  fibrin  which  exudes  is  verj^  variable, 
and  upon  this  factor  the  appearance  of  the  inflammatory  products 
largely  depends.  Where  free  outpouring  occurs,  large  fleshy 
vegetations  are  seen.  When  veiy  little  occurs,  necrotic  changes 
in  the  endocardium  producing  various  degrees  of  ulceration  may 
predominate  in  the  picture.  Even  small  vegetations  entail 
destruction  of  the  endocardium.  Larger  growths  have  a  deeper 
origin  and  cause  relatively  greater  destruction  of  tissue.  A 
combination  of  fungating  and  ulcerating  lesions  is  the  rule  in 
the  severe  forms.  The  latter  may  produce  valvular  perfora- 
tion, and  even  destruction  of  the  underlying  myocardium.  (See 
Fig.  6.)  Occasionally,  necrotic  areas  without  ulceration  or  foci 
of  suppuration  occur.  The  vegetations  vary  greatly  in  appear- 
ance; at  times  soft,  friable,  gelatinous,  white,  reddish  or  yellow 
masses  with  adhering  blood-clots;  again,  the  well-known  cauli- 
flower growths  are  seen.     In  cases  in  which  friction  has  been 

'  Sicard  (32  cases,  Presbyterian  Hospital,  New  York):  Amer.  Jour.  Med.  Sci.,  Nov.,  1904. 


Fig.  3. — Acute  Infective  Mitral  and  Muhal  Endocarditis. 
The  mitral  valve  is  covered  with  large  vegetations.     Several  of  the  chorda.-  tendineaj 
have  been  destroyed  by  ulceration,  only  short  unattached  stumps  remaining.     Vegetations 
are  also  seen  on  the  mural  endocardium.     (Specimen  from  the  Pennsylvania  Hospital.) 


5  STUDIES  IN  CARDIAC  PATHOLOGY 

marked,  long  pendulous  thrombi  maj^  occur.  (See  Fig.  12.) 
Osier  states  that  fibrous  changes,  and  even  calcification,  may 
occur  even  in  acute  cases.  In  such  cases  the  condition  might  be 
confused  with  the  necrotic  changes  seen  in  arteriosclerosis  without 
micro-organismal  infection.^ 

Thrombosis  in  the  auricular  appendages,  especially  if  associated 
with  necrosis,  may  also  at  times  simulate  mycotic  endocarditis. 
Severe  cases  may  perforate  septum  or  heart  itself. 

Simple  endocarditis  occurs  especially  at  the  line  of  valvular 
contact;  the  endocardium  becomes  swollen,  translucent,  and 
somewhat  beaded.  As  the  distended  endothelial  cells  are  detached 
the  blood-plaques  agglutinate  into  small  masses,  which  in  time, 
by  the  addition  of  leukocytes,  develop  into  good-sized  warty 
growths. 

In  severe  cases  the  chordae  tendinese  and  the  papillary  muscles 
are  involved  in  infiltration  and  inflammation.  The  mural  en- 
docardium is  less  often  involved  than  that  of  the  valves,  owing 
to  lessened  functional  activit}'. 

Malignant  endocarditis  may  be  primary  or  secondary;  the 
right-sided  valves  are  attacked  oftener  than  in  the  simple  variety. 
The  vegetations  tend  to  be  more  exuberant  and  friable,  and 
mural  involvement  is  commoner.  Valvular  rupture  (chiefly 
mitral  and  aortic)  is  sometimes  preceded  by  aneurismal  dilatation 
of  the  same,  extending  in  the  direction  of  greatest  pressure.  An 
aneurism  of  the  mitral  valve  generally  involves  the  anterior  flap. 
(See  Fig.  14.)  Rupture  of  the  valves  or  chordae  tendinese,  es- 
pecially when  the  process  is  acute,  is  usually  preceded  by  old 
valvular  disease.  Myocarditis  maj^  occur  by  extension  of  the 
inflammatory  process. 

The  infarcts  of  malignant  endocarditis  perhaps  so  rarely  lead 
to  suppuration  on  account  of  the  low  virulence  of  the  organisms 
to  which  many  cases  owe  their  existence.  Embolic  manifestations 
vary  greatly  in  different  cases.     Sometimes  they  are  very  extensive, 

'  Brit.  Med.  Jour.,  Mar.  7,  1885,  p.  438. 


Fig.  4. — Acute  Infective  Endocakuitis. 
Specimen  showing  large  thrombi  formed  on  the  ulcerated   areas   of  the  aortic  leaflets. 
.VlsD  verj'  small  verruca  in  the  sinu.s  of  Valsalva,  and  some  small  mural  thrombi  between  the 
eolumna;  oarneic  of  the  left  ventricle. 


10  STUDIES  IN  CARDIAC  PATHOLOGY 

as  in  Hoper's  case  of  mitral  stenosis,  in  which  both  femorals, 
the  right  internal  iliac,  the  right  renal,  the  superior  mesenteric, 
and  the  left  brachial  arteries  were  occluded  by  emboli.^ 

The  verrucose  vegetations  of  endocarditis,  which,  as  Hirsch- 
f elder  has  pointed  out,  maj^  form  within  a  few  hours  after  damage 
to  a  valve,  are  in  part  the  result  of  the  action  of  the  blood-stream 
upon  the  fibrinous  exudation.  In  long-standing  cases  contraction 
of  organizing  fibrin  doubtless  plays  a  part  in  the  production  of 
wartlike  vegetations. 

Predisposition. — The  more  frequent  involvement  of  the  left 
side  of  the  heart  has  been  explained  by  the  fact  that  after  birth 
blood-pressure  is  higher  and  oxygenation  greater  than  on  the  right. 
The  former,  as  the  result  of  stress  and  trauma,  favors  the  localiza- 
tion of  micro-organisms,  the  latter  favoring  both  localization  and 
growth. - 

In  237  cases  of  congenital  endocarditis  Rauchf uss  found  the  lesions  right-sided 
in  192.  The  relative  frequency  of  right-sided  lesions  in  fetal  life  was  ascribed  by 
Rokitansky  to  the  effect  of  congenital  malformations,  a  belief  which  subsequent 
investigation  has  corroborated.  Yet  despite  the  fact  that  this  predisposition 
exists,  the  engrafting  of  an  acute  endocarditis  upon  a  congenital  lesion  is  not 
common,  owing  to  the  fact  that  malignant  endocarditis  is  a  disease  of  middle 
life,  an  age  which  the  subjects  of  developmental  heart  lesions  do  not,  as  a  rule, 
attain.'  G.  C.  Robinson^  has  collected  17  cases  of  endocarditis  and  congenital 
malformation,  adding  two  cases  thereto,  and  omitting  those  in  whicli  the  mal- 
formation was  limited  to  the  valves.  In  11  cases  there  was  deficiency  of  the 
interventricular  septum,  and  in  6  of  these  pulmonary  valvular  obstruction. 
Fig.  76  was  from  one  of  the  cases  published  by  Robinson.  Fig.  77  also  illustrates 
the  coincidence  of  infectious  endocarditis  and  congenital  defect. 

Embolic  manifestations  in  the  lung,  spleen,  kidneys,  etc.,  are  much  more 
frequent  in  malignant  or  "infective"  endocarditis  than  in  the  simple  type. 
Among  64  cases  of  the  former,  Glynn  found  44  instances ;  among  64  of  the  latter, 
only  18.'' 

iHoper:   Lancet,  Aug.  18,  1906. 

-  Wadsworth:  Jour.  Infect.  Dis.,  1909,  p.  279. 

'  Malignant  endocarditis  is  rare  in  childhood.  The  statistics  of  StefTen,  Von  Dusoh, 
Hochsinger,  and  Weil  show  that  62  per  cent,  are  of  the  simple  variety,  and  involve  the  mitral 
valve.  Endocarditis  is  rare  in  infants.  Holt  failed  to  find  any  instance  in  1000  autopsies 
on  children  under  three  years;  Steffen,  in  45  cases,  found  only  .5  in  the  first  year  of  life;  Hoch- 
singer, in  .53  cases,  only  one  in  the  first  year  of  life;  v.  Dusch,  in  45  cases,  5  between  eight 
months  and  three  years;  Sutiagin,  in  108  cases,  11  in  the  first  year  of  life. 

■*  G.  C.  Robinson:   Bull.  Ayer  Clinical  Laboratory,  Pennsylvania  Hospital,  1905. 

5  Lancet,  April  18,  1903,  p.  1073. 


Fig.  .5. — iSuBACuxE  Infective  Endocarditis. 
Showing  large  thrombotic  mas.ses  almost  completely  occluding  the  aortic  orifice.     There 
i.s  marked  left  ventricular  hypertrophy,  and  sclerotic  patches  are  seen  on  the  aorta  above  the 
sinus  of  Valsalva. 


12  STUDIES    IN    CARDIAC    PATHOLOGY 

Pathogenesis. — Anj^  infectious  disease  may  be  accompanied 
or  followed  by  an  endocarditis,  which  may  be  homologous,  heter- 
ologous, or  due  to  a  mixed  infection.  A  predisposition  to  it  is 
to  be  found  in  the  minute  endothelial  lesions,  which  are  naturally 
commonest  where  pressure  or  friction  is  greatest — on  the  mitral 
valve.  When  this  valve  is  insufficient,  the  right  heart  may  be 
more  likely  to  develop  acute  endocarditis,  as  in  a  case  described 
by  Marini.^  The  youthful  endocardium  is  much  more  suscep- 
tible to  infection  than  that  of  advanced  years,  as  Church's  statistics 
of  700  cases  show:'- 

1  to  10  years 80  per  cent. 

10  "  20  "  69 

20  "  30  "  62 

.30  "  40  "  .?0 

40  "  .50  "  21 

Further  corroboration  is  to  be  found  in  the  well-known  fact  that 
in  the  rheumatic  fever  of  childhood  the  heart  rareh^  escapes  involve- 
ment, whereas  in  adults  this  is  by  no  means  so  unusual  an  occur- 
rence. 

Dunii'^  in  300  cases  of  rheumatic  arthritis  at  the  Children's  Hospital  in 
Boston  found  evidences  of  endocarditis  in  140,  and  of  pericarditis  in  58.  Two 
hundred  and  eighty-one  at  some  time  in  the  attack  showed  evidences  of  endo- 
carditis, so  that  only  19  in  all  escaped  entirely.  Mitral  insufficiency  was  noted 
70  times,  a  double  mitral  lesion  56  times.  The  140  cases  were  admitted  as 
"endocarditis,"  there  being  other  evidences  of  disease  at  that  time.  Thus  60 
per  cent,  of  the  cases  showed  distinct  evidences  of  endocarditis  at  a  time  when 
there  were  no  arthritic  manifestations. 

The  tendency  of  certain  organisms  to  attack  the  endocardium  is  well  exem- 
plified by  Lenhartz's  results:  In  a  study  of  226  cases  of  general  sepsis,  there  were 
38  cases  of  malignant  endocarditis.  In  149  cases  of  sepsis  due  to  the  strepto- 
coccus pyogenes  there  were  but  6  cases  of  endocarditis.  In  other  words,  the 
.streptococcus  is  the  most  common  cause  of  sepsis,  in  scarlatina,  the  puerperium, 
etc. ;  yet,  proportionately,  endocarditis  was  much  more  common  in  the  cases  due 
to  the  other  organisms.  On  the  other  hand,  95  per  cent,  of  the  staphylococcus 
cases  showed  endocarditis.*  (His  investigations  revealed:  staphylococcus  10, 
pneumococcus  10,  streptococcu?  16,  gonococcus  1.) 

'  Marini:   Gazz.  degli  ospedaU,  1907,  No.  24.  -St.  Bart.  Hosp.  Report,  -\xiii. 

'  Dunn:  ,Jour.  Amer.  Med.  Assoc,  1907,  p.  49:^. 

■'  Lenhartz,  quoted  by  Reye:  Jahrb.  d.  Hamburger  Staatskrank.  Anst.,  190.5,  p.  224. 
(The  valvular  involvement  in  these  cases  was  as  follows:  Mitral,  18:  aortic,  11;  both,  2. 
Tricuspid,  4;  puhnonic,  2;  aortic  and  jjulmonic,  1.) 


ACUTE    ENDOCARDITIS  13 

The  researches  of  Prudden/  Rosenbach,'^  Wyssokowitch/*  and 
Rosenow  "*  have  demonstrated  the  fact  that  endocarditis  is  more 
apt  to  develop  on  an  endocardium  which  has  been  previously 
injured  or  diseased  than  on  a  normal  one.  Goodhart '"  found  ap- 
parently antecedent  valvular  thickening  in  61  out  of  69  cases. 
A  large  number  of  different  organisms  have  from  time  to  time  been 
described  as  the  causative  factor  of  endocarditis.  "The  colon, 
Friedlander,  typhoid,  diphtheria,  influenza  organisms,  the  meningo- 
coccus, the  tubercle  bacillus,  the  bacillus  pyocyaneus,  unrecognized 
species,  others  little  known  but  described  as  the  bacillus  endo- 
carditis griseus,  the  micrococcus  rugatus,  the  micrococcus  cap- 
sulatus  of  Weichselbaum,  the  bacillus  pyocyaneus  fetidus  (Fasset), 
the  diplococcus  tenuis  (Klemperer) — these  and  other  organisms 
have  been  credited  with  producing  the  condition"  (Wadsworth "). 
At  present  there  seems  to  be  a  tendency  to  regard  many  of  these 
diverse  and  little  known  organisms  as  atypical  forms  of  well- 
known  varieties,  such  as  the  streptococcus.  The  pneumococcus, 
the  staphylococcus,  the  streptococcus,  and  the  gonococcus  are 
undoubtedlj^  the  most  freciuent  causes  of  malignant  endocarditis. 
"Bacterial  species  comparatively  benign  in  other  parts  of  the  body 
prove  serious  and  fatal  in  endocarchal  lesions"  (Wadsworth). 

Among  50  cases  of  pneumococcus  endocarditis,  25  per  cent, 
showed  old  lesions  upon  which  the  recent  infection  had  become 
engrafted  (Preble). 

Although  the  difference  between  simple  and  malignant  endo- 
carditis is  nearly  always  only  one  of  degree,  yet  certain  infections 
have  a  marked  tendency  to  cause  definite  types.  Thus  rheumatic 
fever  and  chorea,  so  frequently  the  cause  of  simple  endocarditis, 
rarely  cause  the  malignant  variety;  whereas  with  pneumonia 
and  puerperal  sepsis  the  reverse  is  the  case.     The  mere  fact  that 

'  Prudden:  Am.  Jour.  Med.  Sci.,  1887. 

*  Roscnbach:  Arch.  f.  exper.  Path.,  1878. 

'  Wyssokowitch :  Virchow's  Arch.,  1886,  p.  301. 

■•  Rosenow:  Jour.  Infect.  Dis.,  vi,  1909,  p.  245. 

'Goodhart:  Tran.s.  London  Patli.  Soc,  xxxiii,  p.  52. 

"  Wadsworth:  .Med.  Record,  Dec.  28,  1907. 


14  STUDIES    IN    CARDIAC    PATHOLOGY 

endocarditis  complicates  a  disease  is,  of  course,  no  indication  that 
this  is  not  due  to  a  secondarj^  infection  with  some  other  species 
of  organism.  For  example,  the  pyogenic  cocci  are  generally  the 
cause  of  endocarditis  in  diphtheria  and  tuberculosis,  although 
both  the  Klebs-Loffler  and  the  tubercle  bacillus  have  been 
shown,  both  clinically  and  experimentally,  to  possess  the  faculty 
of  producing  endocardial  inflammation.  However,  we  must  not 
forget  that  "the  organism  isolated  from  an  ulcerative  case  may 
experimentally  in  one  case  animal  give  rise  to  an  ulcerative  form 
of  endocarditis,  while  in  another  animal  of  the  same  species 
simple  endocarditis  may  result."' 

Sometimes  the  experimental  injury  of  valves  in  animals  has 
been  followed  by  lesions  similar  to  those  of  malignant  endocarditis; 
although  not  the  ulcerative  type,  which  appears  to  occur  only 
when  infection  is  also  present.  It  is  conceivable,  therefore,  that 
valvular  rupture  might  give  a  similar  picture  in  man.  Practically, 
however,  malignant  endocarditis  means  a  severe  type  of  infection, 
localized  either  by  means  of  the  general  blood-stream  or  the 
coronary  arteries.  Slight  local  injur j^,  such  as  the  application 
of  nitrate  of  silver,  is  enough  to  determine  the  focus  of  the  infection 
on  the  endocardium  (Prudden) .  The  mycotic  origin  of  practically 
all  cases  of  verrucose  endocarditis  is  generally  admitted.  Articles 
bearing  on  this  subject  are  very  numerous.  Thus  Bartel-  studied 
23  cases  and  concluded  that  all  cases  of  verrucose  endocarditis 
have  such  an  origin;  the  extent  of  the  lesion  varying  with  the 
duration  and  virulence  of  the  infection,  and  with  the  amount  of 
individual  tissue  resistance. 

Rheumatic  fever  is  by  far  the  most  prohfic  source  of  "simple" 
endocarditis,  from  80  to  90  per  cent,  of  this  variety  being  due  to 
this  cause.  Rheumatic  fever  is  now  universally  regarded  as  an 
infection,  and  although  the  exact  micro-organism  which  causes 
it  has  not  yet  been  definitely  determined,  the  majority  of  cases 

'  Beattie  and  Dickson:   Special  Pathology,  1909,  p.  12. 
=  Bartel:  Wien.  klin.  Woch.,  Oct.  10,  1901. 


Fig.  6. — Acute  Infective  Endocarditis. 
Showing  extensive  ulceration  of  the  aortic  valves.     About  the  center  of  the  aortic  orifice 
a  match-stick  projecting  from  a  thrombotic  mass  indicates  the  course  of  the  perforation  in  the 
aortic  leaflet.     fSpecimen  from  the  Philadelphia  Hospital.) 


16  STUDIES    IN    CARDIAC    PATHOLOGY 

owe  their  origin  to  various  organisms  of  the  streptococcus  group. 
A  diplococcus  described  by  Wasscrmann,  and  later  by  Poynton 
and  Paine,  Longcope,  and  otliers,  seems  to  be  responsible  for  a 
considerable  number  of  the  cases.  According  to  Beattie  and 
Dickson,  the  diplococcus  rheumaticus,  which  is  a  common  in- 
habitant of  the  mouth  and  intestines,  may,  under  certain  condi- 
tions of  increased  virulence  on  the  part  of  the  germ,  or  decreased 
resistance  on  the  part  of  the  host,  produce  the  infection.  They 
suggest  that  some  of  the  cases  of  endocarditis  occurring  in  rheu- 
matic fever,  Bright's  chsease,  scarlatina,  and  chorea  may  thus 
arise.-' 

Sibson  in  325  cases  of  rheumatic  fever  found  endocarditis  in  130,  both 
endocarditis  and  pericarditis  in  54,  and  the  latter  alone  in  9.  Seventy-nine  per 
cent,  of  the  cases  with  previous  endocardial  lesions  developed  an  acute  infection, 
whereas  of  those  with  no  antecedent  disease  only  56  per  cent,  were  afflicted. 
Among  270  cases  of  rheumatic  fever  studied  by  McCrae,  85,  or  32  per  cent.,  had 
undoubted  organic  endocardial  disease — mitral,  95  per  cent.;  aortic,  23  per 
cent. ;  both  valves,  18  per  cent.  Of  the  85  cases  of  mitral  involvement,  54  were 
insufficiency,  3  obstruction,  and  8  a  double  lesion.  At  St.  Thomas'  Hospital 
among  535  cases  of  rheumatic  fever  the  mitral  valve  was  involved  in  97  per  cent., 
the  aortic  in  12  per  cent.,  the  aortic  alone  in  3  per  cent.  There  were  apparently 
no  cases  of  malignant  endocarditis  in  McCrae's  series.  He  found  in  addition  to 
the  above  mentioned  cases  78  (28  per  cent.)  in  which  organic  disease  was  doubt- 
ful; of  these,  60  were  discharged  with  murmurs  of  uncertain  cause.  In  136  cases 
of  rheumatic  fever  reported  by  Latham,  90  showed  cardiac  involvement — 63 
endocarditis,  7  pericarditis,  11  both,  9  doubtful  cases.  Among  150  cases  of 
infective  endocarditis  at  St.  Bartholomew's  Hospital,  Horder  found  that  72  gave 
a  history  of  acute  or  subacute  rheumatic  fever  or  chorea,  10  of  scarlatina,  7  of 
gonorrhea,  4  of  typhoid  fever,  4  of  malaria,  2  of  syphilis,  2  of  influenza,  1  of 
exophthalmic  goiter,  1  of  dysentery,  1  of  pneumonia.  In  53,  no  history  of  pre- 
ceding disease  could  be  obtained.  Phillips  in  210  cases  of  acute  rheumatic  fever 
found  63  cases  of  undoubted  endocarditis — mitral  56,  aortic  13,  both  11.  Among 
288  cases  of  rheumatic  arthritis  in  Christiania  there  were  heart  comphcations  in 
33  per  cent. ;  and  of  242  cases  of  heart  disease  there  was  a  history  of  rheumatic 
fever  in  46.5  per  cent.,  of  syphihs  in  9.2  per  cent.,  influenza  in  2.5  per  cent.  Of 
the  chorea  cases  31  per  cent,  showed  cardiac  lesions.-  Among  30,000  patients, 
Litten  found  400  cases  of  endocarditis.     In  35  per  cent,  of  these  the  cardiac 

'  Details  regarding  the  bacteriology  may  be  found  in  Bulloch's  article,  "Rheumatic  Fever," 
vol.  ii,  part  9,  of  the  new  edition  of  Allbutt  and  Rolleston's  System  of  Medicine,  1906,  vol.  ii, 
part  i,  p.  594. 

'  Thiis:  Norsk  Mag.  f.  Laegevedenskaben,  Oct.,  1909,  Ixx. 


ACUTE   ENDOCARDITIS  17 

lesion  was  certainly  due  to  rheumatic  fever.  In  30  per  cent,  other  definite 
causes  could  be  as.signed,  and  in  the  remaining  30  per  cent,  no  etiologic  factor 
was  demonstrable.'  Forssner-  found  that  45  out  of  74  cases  of  acquired  heart 
disease  in  children,  and  32  among  60  in  adults,  resulted  from  rheumatic  fever. 
Romberg  in  670  cases  of  valvular  disease  at  the  Leipzig  chnic  found  that 
58.9  per  cent,  were  rheumatic  in  origin.  Among  258  cases  of  acute  endo- 
carditis in  children  Perroud^  found  it  associated  with  different  infectious 
processes  as  follows:  rheumatic  fever,  150;  chorea,  39;  tuberculosis,  15; 
scarlatina,  12;  pneumonia,  7;  measles,  7;  cUphtheria,  7;  typhoid  fever,  4 ;  dys- 
entery, 3;   erythema  nodosum,  2;  undetermined,  12. 

In  a  study  of  1,369  clinical  reports  of  scarlatina  cases,  Rochely  found  no 
acute  endocarditis,  nor  did  Reimer  among  48  autopsies.  The  endocarditis  of 
scarlatina  and  variola  is  said  to  be  generally  of  the  simple  variety.  In  550  cases 
of  scarlatina,  Beatty""  found  7  cases  of  endocarditis.  It  has  also  been  reported 
following  vaccination.  Barbier  in  45  diphtheria  autopsies  found  23  cases  of 
cardiac  thrombosis  (chiefly  right  auricular) ;  these  cases  were  considered  as 
resulting  from  mural  endocarditis  due  to  the  "diplococcus  hemophilus  per- 
lucidus."  Cohn^  has  reported  a  fatal  case  of  endocarditis  following  chancroid, 
both  lesions  culturally  exhibiting  the  staphylococcus  pyogenes  aureus. 

Pneumonia  heads  the  list  of  all  diseases  complicated  by  severe 
endocarditis  (Osier).  Acute  endocarditis  has  been  attributed  to 
pneumonia  as  follows: 


Harbitz 

Traux 

Kanthack  and  Tickell 14 

Lenhartz 

Jackson 

Waller 

Weichselbaum 

O-sler 54 


2  out  of 

9  cases 

8    "    " 

22 

14    "    " 

34     ' 

9    "    " 

43     ' 

1    "    " 

6     ' 

14    "    " 

84     ' 

5    "     " 

38     ' 

1    "     " 

5     • 

1    "     " 

21     ' 

6    "    " 

33     ' 

54    "    " 

209     ' 

'      (Ulcerative) 

Total 115  out  of  .504  cases  (22  per  cent.) 

Preble,*^  basing  his  statement  on  collected  statistics,  states 
that  the  pneumococcus  is  something  over  twice  as  apt  to  involve 
the  aortic  valves  as  other  bacteria,  and  about  one-third  as  apt 

1  Deut.  mod.  Woch.,  May  22,  1902. 

2  Nordiskt  Med.  Arkiv.,  1909,  xli,  No.  3. 

'  Perroud :  Weill's  Traits  clinique  des  mal.  du  cocur  chcz  les  enfants. 
*  Dublin  Jour.  Med.  Sci.,  1907. 
'Cohn:  Jour.  Amer.  Med.  A.ssoc,  1909,  47,  p.  1106. 

'Preble;  "  Pneiiiiiotiia  and  Pneumococcic  Infections,"  Chicago,  lOO.'),  p.  133. 
2 


18  STUDIES    IN    CARDIAC    PATHOLOGY 

to  involve  the  mitral,  while  it  attacks  the  tricuspid  twenty  times 
as  often.  The  last  fact  is  probably  influenced  by  the  special 
physical  conditions  which  result  from  pulmonary  consolidation. 
Pneumococcus  endocarditis  is  twice  as  common  in  women  as  in 
men,  and  about  three-fourths  of  the  cases  are  ulcerative  in  char- 
acter, while  lesions  of  the  right  heart  are  more  common  than 
in  other  varieties  of  endocarditis.  The  aortic  and  pulmonary 
valves  are  involved  more  frequently  than  in  other  forms  of  the 
disease.  Among  32,894  cases  of  pneumonia  collected  from  the 
literature,  149  cases  of  acute  endocarditis  were  reported,  and 
among  2,722  pneumonia  autopsies  acute  endocarditis  occurred 
158  times. ^  The  pneumococcus  generally  produces  large,  isolated, 
friable,  pedunculated  vegetations,  which  on  being  detached  leave 
but  a  small  ulcerated  surface.  The  streptococcus,  on  the  other 
hand,  often  causes  extensive  ulceration  covered  by  small  verrucose 
excrescences,  at  times  hemorrhagic  and  necrotic.  Billings,'  in 
a  study  of  14  cases  of  chronic  infectious  endocarditis,  found  11 
due  to  the  pneumococcus,  3  to  the  streptococcus.  Culturally  the 
former  organism  showed  distinct  differences  from  the  type  which 
ordinarily  causes  pneumonia.  The  origin  of  infection  was  as 
follows:  Pneumonia  1,  tonsillitis  2,  alveolar  abscess  2,  influenza  1, 
no  discoverable  cause  8 .  We  are  thus  gradually  coming  to  realize 
the  fact  that  relativelj'  unimportant  infections  of  the  nares,  naso- 
pharynx, ears,  mouth,  gums,  etc.,  may  be  the  portal  of  entrance 
for  the  most  severe  t.ype  of  endocardial  inflammation. 

As  has  been  intimated,  pneumococcus  endocarditis  is  apt  to 
be  rapidlj^  fatal.  Acute  cases  do  not  usually  last  over  three 
months,  although  Frankel  has  reported  a  case  of  pneumococcus 
endocarditis  lasting  six  months.^  In  Rosenow's  experiments 
the  lesions  were  generally  progressive,  though  healing  did  occur. 
He  states  that  "a  close  relationship  exists  between  the  biologic 
characters   of   the   bacteria   and  their   abihty  to  produce  endo- 

'  Statistics  collected  by  the  author. 

'-  Billings;  Arch.  Int.  Med.,  1909,  iv,  No.  5.  '  Frankel:   Deut.  med.  Woch.,  1900. 


Fio.  7. — Acute  Infective  Endocarditis. 
The  aortic  leaflets  are  thickened,  shriveled,  perforated,  and  show  extensive  ulcerative 
tissue  destruction  with  little  thrombosis.     Beneath  the  aortic  leaflets  the  ulceration  is  begin- 
ning to  extend  downward  toward  the  mitral  valve. 


20  STUDIES  IN  CARDIAC  PATHOLOGY 

carditis  in  the  class  of  cases  observed."  " The  bacteria  isolated, 
while  having  little  or  no  pathogenic  power  to  animals,  and 
being  susceptible  to  phagocytosis,  present  definite  evidence  of 
being  immunized  against  the  antibodies  of  the  individual  host, 
thereby  perhaps  overcoming  the  resistance  of  the  latter." 

In  a  series  of  cases  of  pneumococcus  endocarditis  studied  by 
Rosenow^  the  mitral  and  tricuspid  valves  were  mostly  diseased, 
a  state  of  affairs  which  he  attributes  to  the  presence  of  capillaries 
in  these  valves  favoring  embolism. 

The  exact  distribution  in  Preble's  cases  of  endocarditis  in 
pneumonia  was  as  follows: 

Per  Cent. 

Aortic  only 56  39.7 

Mitral  only 40  28.3 

Aortic  and  mitral 20  14.1 

Tricuspid  only 12  8.5 

Pulmonary  only 5  3.5 

Aortic,  mitral,  and  tricuspid 5  3.5 

Mitral  and  tricuspid 2  1.4 

Aortic  and  tricuspid 1  0.7 

In  Jurgensen's  collection  we  find: 

Peh  Cent. 

Aortic  only 18.7 

Mitral  only G6.3 

Aortic  and  mitral 9.2 

Tricuspid  only 0.4 

Pulmonary  only 2.3 

Aortic,  mitral,  and  tricuspid 1.0 

Mitral  and  tricuspid 1.8 

Aufrecht  gives  the  following  data  regarding  the  distribution 
in  relation  to  age,  as  well  as  the  distribution  of  pneumonia  itself: 

Pneumococcus 
Number   Endocarditis.  Pneumonia. 

Decade.  of  Cases.     Per  Cent.  Per  Cent. 

First 2 1.4  1  6.8  1 

Second 8.  .  .  .   5.7  i  11.9  22.2  j- 58 

Third 15 ...  .  lO.S  J  29.0  J 

Fourth •. 42.  .  .  ..30.4  \  17.0  ] 

Fifth 27.  .  .  .19.5  [70.9  13.0  1-35.5 

Sixth 29.  .  .  .21.0  J  5.5  J 

Seventh  and  over 15 ...  .  10. S  6.0 

Chorea,  another  disease  which  has  lately  been  added  to  the 
list  of  infections,  is  a  common  cause   of  endocarditis.     Thayer^ 

'  Rocenow;  Jour.  Infect.  Dis.,  1909,  p.  245.     -  Thayer:  Jour.  Am.  Med.  Assoc,  1906,  p.  1352. 


ACUTE    ENDOCARDITIS  21 

in  689  cases  of  chorea  found  cardiac  murmurs  in  235  (40.5 
per  cent.);  cardiac  involvement  was  more  frequent  during  second 
attacl'vis  and  in  those  cases  which  had  had  rheumatic  fever. 
Forssner^  was  able  to  trace  the  subsequent  history  of  28  chorea 
cases  for  periods  of  from  fifteen  to  twenty-two  years,  and  found 
that  5  showed  pronounced  heart  disease,  while  7  had  died  of  it. 
Among  35  cases  of  rheumatic  fever  thus  followed,  17  developed 
heart  disease  and  7  had  died  as  a  result. 

The  importance  of  the  gonococcus  as  a  cause  of  acute  endocard- 
itis has  been  justly  much  emphasized  since  the  cultural  demon- 
stration of  the  organism  in  the  blood  during  life,  bj^  Thayer  and 
Blumer  in  1895.  Before  that  time  the  organism  had  been  found 
on  the  valves  bj^  v.  Ley  den,  and  even  as  far  back  as  the  time  of 
Ricord  and  Brandes  the  association  of  endocarditis  and  urethritis 
had  been  noted.  In  1903  Kuelbs-  collected  from  the  literature 
49  cases  of  endocarditis  due  to  the  gonococcus,  in  28  of  which  the 
aortic  valve  was  affected,  the  mitral  in  8,  the  pulmonary  in  6, 
and  the  tricuspid  in  1.  Gonococcus  endocarditis  is  often  very 
severe,  producing  large  vegetations,  deep  and  extensive  ulceration, 
and  at  times  myocardial  involvement.  Emboli  appear  to  be 
infrequent.  It  more  freciuently  complicates  gonorrhea  in  the 
male  than  in  the  female.  Although  disease  of  the  mj'ocardium 
and  endocardium  may  be  caused  by  this  organism,  endocardial 
disease  is  more  commonly  the  result  of  this  infection.  Sometimes, 
however,  mild  attacks  do  occur,  and  in  these  the  mitral  valve  is 
more  often  involved.  The  severe  form  is  usually  associated  with 
other  metastatic  manifestations,  such  as  arthritis,  etc.  At  autopsy 
grayish-red,  easily  detachable  vegetations  are  usually  found  near 
the  margins  of  the  valves,  which  occasionally  extend  to  the  en- 
docardium beyond.  The  gonococcus  is  sometimes  tinctorially, 
less  often  culturally,  demonstrable.  Mixed  and  secondary  in- 
fections occasionally   occur.     Valvular  involvement  is  generally 

'  Forssru'r:  .l.'iiiilj.  f.  J<inilcrlii'ill<.,  Jan.,  1910,  Ixxi. 
-  Kudb.s:   Wicn,  kliii.  WoiJ].,  l!l()7,  .\x. 


22  STUDIES  IN  CARDIAC  PATHOLOGY 

not  multiple.  A  lethal  outcome  is  the  rule,  although  some  cases 
recover.  Irons^  states  that  there  are  now  on  record  some  120 
cases  of  gonorrheal  endocarditis,  in  several  of  which  pericarditis 
was  also  found.  The  infarcts  rarely  suppurate  and  petechise 
are  infrequent. 

Although  the  occurrence  of  endocarditis  and  tuberculosis 
coincidently  is  by  no  means  as  exceptional  as  was  once  supposed, 
and  although  verrucose  endocarditis  has  been  experimentally 
produced  by  the  tubercle  bacillus,-  yet  true  tuberculous  endo- 
carditis is  distinctly  rare.  MarshalP  makes  five  classifications 
to  cover  the  relationship  of  the  two  conditions.  (1)  Miliarj^ 
tuberculosis;  (2)  true  tuberculous  endocarditis;  (3)  tuberculous 
cardiac  thrombosis;  (4)  tuberculous  endocarditis  secondarj^  to 
mj^ocarditis;    (5)  toxic  tuberculous  endocarditis. 

Unfortunately  the  majority  of  available  statistics,  including 
my  own,''  which  deal  with  the  occurrence  of  recent  endocarditis 
in  pulmonaiy  tuberculosis,  give  no  information  regarding  the 
microscopic  findings  or  bacteriologic  examinations.  The  frequency 
with  which  this  condition  has  been  encountered  is  shown  in  the 
appended  tabulation : 

Tuberculous  Recent 

Endocarditis.  Per  Cent. 


Teissier 100  32  32.0 

Schultze 6,937  67  0.966 

Osier 216  12  ',  r, 

Kidd 500  6  1.2 

Norris 1,764  16  0.9 

Fenwick 1,560  13  0.7 

Otto 185  4  3.1 

Dittrich 403  1  0.24 

11,665  151  1.2 

Doubtless  in  the  majority  of  the  above  cases  the  acute  endocarditis  was  due 
to  other  causes  than  the  tubercle  bacillus.  In  one  of  Osier's  cases  fresh  tubercles 
were  found  upon  the  mitral  leaflet,  but  no  tubercle  bacilli  could  be  demonstrated 
in  the  sections.  Kidd  and  Councilman  also  failed  to  find  them.  Even  when 
the  bacilli  can  be  demonstrated,  it  is  perfectly  possible  that  their  presence  is 

1  Irons:  Arch.  Int.  Med.,  1910,  p.  601. 

-  Michaelis  and  Blum:  Deut.  med.  Woch.,  1895. 

'  Marshall:  Johns  Hopkins  Hospital  Bull,  1905,  p.  303. 

■*  Norris:  .4m.  Jour.  Med.  Sci.,  Oct.,  1904. 


ACUTE    ENDOCARDITIS  23 

simply  accidental,  as  a  roughened  endocardium  would  present  a  favorable 
ground  for  the  lodgment  of  micro-organisms  carried  thence  by  the  blood-stream. 

Slight  degrees  of  simple  sclerotic  endocarditis  are  met  with  very  commonly 
in  pulmonary  tuberculosis,  aiid  are  presumably  due  to  the  toxemia  which  is 
present  in  the  chronic  variety  of  this  disease.  The  researches  of  Auclair  ^  have 
shown  that  the  metabolic  products  of  the  tubercle  bacillus  possess  sclerogenetic 
as  well  as  necrogenetic  properties,  which  would  readily  account  for  the  endo- 
cardial thickening.  Boinet  and  Romary's  -  experiments  indicate  that  bacterial 
toxin,  even  in  the  absence  of  bacteria  themselves,  and  without  the  addition  of 
trauma,  are  capable  of  producing  changes  in  the  endocardium  and  aorta. 

"Ectasine,"  the  vasodilatory  substance  which  Bouchard  has  shown  to  be  a 
constituent  of  the  tuberculous  toxin,  by  producing  vascular  relaxation  would 
favor  diapedesis  of  the  leukocytes,  thus  paving  the  way  for  sclerogenous  pro- 
cesses. 

Teissier  has  enunciated  the  behef  that  mitral  stenosis  is  frequently  produced 
by  the  prolonged  action  of  the  tuberculous  toxin  upon  the  endocardium,  which 
in  time  results  in  a  narrowing  of  the  valvular  orifice,  and  states  that  this  form  of 
valvular  lesion  exerts  an  inhibitory  effect  upon  the  pulmonary  disease.  If  such 
an  inhibition  exists,  it  is  more  probably  due  to  the  increased  resistance  which  the 
bodily  tissues  have  acquired  through  the  prolonged  presence  of  the  toxin  in  the 
system  than  to  the  mechanical  action  of  the  stenosis.  Chartier  ^  remarks  that 
this  sclerogenous  tendency  is  not  tuberculosis,  but  the  index  of  immunity  versus 
tuberculosis. 

A  tuberculous  process  may  of  course  be  engrafted  upon  a  pre-existing  val- 
vulitis of  different  etiology,  or  the  condition  may  be  reversed.  An  interesting 
case  has  been  reported  by  Debove;*  an  incUvidual  aged  thirtj^-four  years  died 
in  a  cachectic  condition,  and  at  autopsy  tubercle  bacilli  were  found  in  the  blood 
and  in  the  mitral  vegetations,  no  tuberculous  lesions  being  encountered  else- 
where. 

Heller,  Cornil,  and  Kundrat  were  among  the  first  to  describe  tuberculous 
endocarditis,  but  the  credit  of  the  first  definite  and  accurate  report  of  this  condi- 
tion belongs  to  Tripier,  who,  in  a  case  of  miliary  tuberculosis,  found  a  small 
nodule  on  the  anterior  leaflet  of  the  mitral  valve  which  showed  the  characteristic 
cellular  changes  upon  microscopic  examination,  as  well  as  the  tubercle  bacillus 
itself.  Some  time  afterward  v.  Leyden  reported  four  similar  cases,  in  one  of 
which  the  condition  was  diagno.sticated  ante  mortem.  Lion,  and  Londe  and  Petit 
demonstrated  tubercle  bacilli  in  the  valvular  endocardium,  but  derived  negative 
re.sults  from  inoculation  experiments.  Similar  results  were  obtained  by  Etienne, 
de  Thiry,  Benda,  Poncet  and  Dor,  Ferrand  and  Rathery.  Michaelis  and  Blum 
were  the  first  to  succeed  with  inoculation  by  producing  tuberculous  endocarditis 
in  rabbits;    and,  finally,  Braillon  and  Jousset  demonstrated  tubercle  bacilli  in 

'  Auclair:  Arch.  mcd.  cxpor.,  1900,  p.  189. 
2  Boinet  and  Romary:  Ibid.,  1S57,  p.  902. 
'  Charlior:   Rev.  do  la  Tubcrculosc,  Feb.,  1904. 
'  Debovo:  Oa/„  deis  Hopilaiix,  190.'i. 


24  STUDIES    IN    CARDIAC    PATHOLOGY 

the  blood  of  a  man  dying  of  primary  tuberculous  endocarditis,  the  only  other 
evidences  of  this  infection  having  been  a  few  pleural  adhesions.  Tuberculous 
endocarchtis  usually  assumes  a  verrucose,  but  sometimes  an  ulcerative  form. 
According  to  Benda,  the  majority  of  the  cases  have  their  origin  in  a  miliary  in- 
fection, which  happens  to  become  localized  upon  the  valves,  being  in  this  respect 
analogous  to  the  condition  described  by  this  author  as  tuberculous  endangeitis. 
In  searching  through  the  records  of  the  Philadelphia  Hospital  among  1,606 
tuberculosis  autopsies  two  cases  were  found  which  were  designated  as  "tuber- 
culous endocarditis";  small  tubercles  had  been  found  upon  the  valves,  but  ap- 
parently no  microscopic  examination  had  been  made.^ 

The  bacillus  typhosus  is  one  of  the  rarer  causes  of  endocarditis. 
When  endocarditis  occurs  in  typhoid  fever,  it  generally  results 
from  mixed  infections.  Experimentally  endocardial  lesions  have 
been  produced  by  the  typhoid  toxin  by  Di  Vecchi.  As  a  rule, 
however,  the  mj'ocardium  suffers  more  in  typhoid  fever  than  the 
endocardium,  just  as  it  does  in  diphtheria  and  in  influenza. 

Acute  endocarditis  in  malaria  is  extremely  rare.  The  mis- 
conception regarding  this  fact  has  been  due  to  the  fact  that  the 
chills  and  fever  of  malignant  endocarditis  have  been  mistaken 
for  plasmodial  infection. 

Subacute,  insidious  endocarditis  occurs  frequently  in  the 
subjects  of  arteriosclerosis,  chronic  valvular,  renal,  or  hepatic 
disease,  also  in  mild  cases  of  rheumatic  fever  or  of  tonsillitis.  A  low 
grade  of  endocardial  inflammation  continues  for  a  long  time,  doing 
more  and  more  valvular  damage,  until  finally  attention  is  called 
to  the  seriousness  of  the  case  by  increasing  fever,  anemia,  or  an 
attack  of  broken  compensation.  Blood-cultures  in  these  cases 
often  yield  streptococci  of  low  virulence  or  of  atypical  appearance. 
Slight  degrees  of  fever  of  prolonged  duration  may  be  constantly 
or  intermittently  present. - 

Chronic  Infective  Endocarditis. — Osier  has  described  a  series 
of  ten  cases,  in  one  of  which  the  process  lasted  thirteen  months. 
Of  course,  it  is  hard  to  differentiate  between  subacute  and  chronic 

'  For  further  bibliographj'  of  tuberculous  endocarditis  see  article  by  the  author  in  Am. 
Jour.  Med.  Sci.,  Oct.,  1904. 

-  See  "901  cases  of  Chronic  Endocarditis  with  Especial  Reference  to  Fever,"  J.  S.  Thacher, 
Am.  Jour.  Med.  Sci.,  ,Tan.,  1906. 


Fig.  8. — Acute  Infective  Endocarditis. 

Clixic^i.  Notes:  Case  of  a  man  aged  twenty-one  years,  with  the  physical  signs  of  aortic 
and  mitral  insufficiency  with  nephritis. 

Pathologic  Notes:  Acute  infective  endocarditis  with  hypertrophy  and  dilatation  of  the 
heart.     Passive  oonKcstion  of  the  lungs,  hver,  etc. 

The  heart  weighs  G70  gm.  The  aortic  leaflets  are  covered  with  large  vegetations  of  recent 
origin.  Similar  although  smaller  vegetations  are  also  found  on  the  left  ventricular  wall  and  upon 
the  mitral  valve.  (Philadelphia  Ho.spital,  vol.  xxi,  p.  2.56.  Physician:  Dr.  J.  Sailor.  Patholo- 
gist: Dr.  D.  J.  Wilson.) 


26  STUDIES    IN    CARDIAC    PATHOLOCxY 

cases.  No  exact  dividing-line  can  be  drawn  between  the  point 
at  which  a  subacute  infection  ends  and  chronicity  begins.  In 
the  above  mentioned  cases,  which  were  all  fatal,  embolic  mani- 
festations occurred  in  four,  blood-cultures  were  sterile  in  three, 
showed  streptococci  in  two,  and  staphylococci  in  one  instance. 

Cultures  made  in  66  cases  from  the  vegetations  and  heart's 
blood  in  107  cases  of  acute  endocarditis  at  the  Pennsjdvania 
Hospital  showed  the  following  micro-organisms: 

Diploeoccus  lanceolatus 10 

Staphylococcus  pyogenes  aureus 10 

Bacillus  coli  communis 9 

Streptococcus  pyogenes 10 

Pneumococcus 3 

Bacillus  typhosus 2 

Micrococcus  citreus 1 

More  than  one  species 6 

Gonococcus 1 

Meningococcus 1 

Bacillus  proteus  vulgaris 1 

A  chromogenic  bacillus 1 

Atypical  streptococcus 1 

Unidentified  species 1 

Sterile  cultures 7 

Contamination 2 

(In  41  no  cultures  were  made.) 

As  compared  with  the  diphtheria  and  the  tubercle  bacillus,  the  staphylo- 
coccus pyogenes  aureus  shows  much  greater  coagulogenetic  power. ^ 

These  107  cases  occurred  among  1,300  general  autopsies.  Valvular  involve- 
ment was  as  follows:  aortic,  25;  mitral,  47;  both,  23;  aortic,  mitral,  and  tri- 
cuspid, 2;  mitral  and  tricuspid,  4;  tricuspid,  3;  pulmonic,  1  (gonococcus);  all 
valves,  2.  Sixty-five  of  these  cases  showed  also  a  chronic  endocarditis,  resulting 
from  previous  infection  (60  per  cent.).  In  nearly  every  instance  the  acute  in- 
fection localized  itself  upon  a  valve  which  had  already  been  diseased. 

At  the  Philadelphia  General  Hospital  among  8,640  autopsies,  acute  endo- 
carditis occurred  as  follows:  aortic,  164;  mitral,  143;  tricuspid,  15;  pulmonic, 
7;   mural  ulcerative,  6;   vegetative,  5. 

At  St.  Bartholomew's  Hospital-  among  19,904  medical  in-patients  there 
were  115  cases  of  infective  endocarditis.  Valvular  involvement  was  as  follows: 
Mitral  only,  38;  aortic  only,  22;  both,  63;  mitral,  aortic,  and  tricuspid,  14; 
mitral,  aortic,  and  pulmonic,  7;  mural  endocarditis — auricular  43,  ventricular  8. 

^  Thorel:  Lubarsch  and  Ostertag's  Ergebnisse  d.  allg.  Path.,  1907,  p.  483. 
=  Horder:   Quart.  Jour.  Med.,  1908,  ii,  289,  324. 


ACUTE    ENDOCARDITIS  27 

Most  of  the  cases  occurred  between  the  ages  of  twenty  and  forty  years,  the  dis- 
tribution between  the  sexes  being  about  equal. 

The  cause  of  death  in  the  last-named  cases  was  as  follows:  Circulatory 
failure,  66;  coma,  23;  sudden  death  from  embolism  or  changes  in  the  heart 
itself, — rupture  of  aneurismal  valves,  septal  perforation,  rupture  of  the  heart, — 
19;  uremia,  18;   exhaustion,  8;   dehrium,  5. 

Embolism  in  endocarditis  was  unrecognized  previous  to  Vir- 
chow's  description;  since  that  time  it  has  been  considered  one  of 
the  most  direful  consequences  of  endocarditis.  Emboh  are  clas- 
sified, first,  according  to  their  origin  as  endogenous  and  exogenous, 
and,  second,  according  to  their  nature  as  simple  or  infective.  In 
a  study  of  250  cases  of  embolism  occurring  in  heart  disease  at 
the  medical  clinic  at  Zurich,  Ginsburg^  found  110  cases  (44  per 
cent.)  in  men,  56  per  cent,  in  women,  the  age  distribution  being  as 
follows : 

10  to  20  years 8  cases,  3.2  per  cent. 

21  to  30  "     33  "  13.2 

31  to  40  "     21  "  8.4 

41  to  50  "     44  "  17.6 

51  to  60  "     : 59  "  23.6 

61  to  70  "     ' 59  "  23.6 

Over   70  "     26  "  10.6        " 

One  hundred  and  ninety-eight  occurred  in  cases  of  endocarditis,  30  in 
cardiac  hypertrophy  and  dilatation,  17  in  myocarditis,  5  in  simple  "cardiac 
insufficiency. "  Among  the  first-named  class  the  mitral  valve  was  diseased  in 
100  cases  (50.8  per  cent.),  the  aortic  in  19  (9.6  per  cent.),  the  mitral  and  aortic  in 
43  (21.7  per  cent.),  the  mitral  and  tricuspid  in  14  (7  per  cent.),  the  mitral,  aortic, 
and  tricuspid  in  17  (8.6  per  cent.),  the  aortic  and  tricuspid  in  1,  and  all  valves  in 
2  instances.  It  will  be  noted  that  the  left  heart  was  the  source  of  emboli  in  79, 
and  the  right  in  13  cases.  The  distribution  of  the  emboli  was  as  follows:  Kid- 
neys, 62;  spleen,  23;  brain,  15;  lungs,  14;  mucosa  of  the  intestines,  3.  Sper- 
ling's statistics  based  on  300  cases  of  endocarditis  are  much  the  same.  In  all, 
embolism  was  noted  in  84  cases ;  in  76  cases  left-sided  lesions  were  the  cause,  the 
distribution  being  as  follows:  Kidney,  57;  spleen,  39;  brain,  15;  digestive 
tract,  5;  skin,  4. 

Clinical  Considerations. — While  some  of  the  severer  cases  of 
acute  endocarditis,  with  hectic  fever,  tachycardia,  cardiac  murmurs, 
and  local  evidences  of  infarction  are  easily  diagnosticated,  the 
le.ss  fulminating  cases  are  too  easily  and  too  often  overlooked. 

'  (liii.shuri;:   Drul.  .\rcli.  f.  kliii.  Med.,  lOOl,  l.\ix,  006. 


28  STUDIES  IN  CARDIAC  PATHOLOGY 

Recent  investigations  have  shown  that  subacute  bacteremia 
with  progressive  endocardial  inflammation  may  go  on  for  weeks 
and  months  while  the  patients  are  still  up  and  about.  From  one 
to  five  months  may  elapse  between  the  onset  of  acute  endocarditis 
and  the  symptoms  pointing  to  valvular  lesions.^  All  autopsy 
statistics  demonstrate  the  frequencj^  with  which  acute  endocarditis 
is  diagnosticated  as  typhoid  fever,  uremia,  chronic  endocarditis, 
pneumonia,  malaria,  influenza,  tuberculosis,  etc.     In  the  hospital 

'  Four  cases  with  three  autopsies,  reported  by  Leclero,  Lessieur,  and  Mouriquand,  Lyon 
Medic,  1906,  No.  5L 

Fig.  9. — Acute  Mural  Endocarditis. 

F.  F.,  female,  aged  eleven  years.  (Philadelphia  Hospital.  Physician:  Dr.  S.  S.  Cohen. 
Pathologist:  Dr.  Funke.) 

Clinical  Notes:  Previous  diseases,  measles,  diphtheria,  typhoid  fever. 

Physical  Examination:  Cyanosis,  dyspnea,  cervical  pulsation,  marked  precordial 
bulging,  with  a  tremendous  heavinp:  pulsation.  Apex-beat  in  the  seventh  interspace  in  the 
anterior  axillary  hne.  A  prondumcil  diastolic  thrill  is  felt  in  the  second  and  third  interspaces. 
Marked  enlargement  of  the  cardiac  dulhicss  to  both  right  and  left.  Two  murmurs  are  heard, 
the  diastolic  being  loudest  at  the  pulmonic  area.  It  is  very  high-pitched  and  transmitted 
down  the  sternum.  A  loud,  somewhat  musical  murmur  is  heard  at  the  apex  and  transmitted 
to  the  axilla,  which  does  not  quite  replace  the  first  sound.  At  the  aortic  area  a  faint  tone  is 
heard  suggestive  of  a  friction  sound.  A  loud  systolic,  probably  tricuspid  murmur  is  noted  at 
theensiform  cartilage.  The  liver  is  enlarged,  but  does  not  pulsate.  Hemoglobin,  4.5  per  cent.; 
erythrocytes,  2, .500,000.  The  urine  contains  albumin  and  hyalin  and  granular  casts.  Death 
occurred  gradually  after  a  considerable  hemoptysis,  and  with  increasing  failure  of  compensation. 

Pathologic  Diagnosis. — Acute  ulcerative  endocarditis  of  the  mitral  leaflets  and  of  the 
posterior  wall  of  the  left  auricle.  Perforation  of  the  pulmonary  leaflet.  Adhesion  of  the  aortic 
leaflets.  Hypertrophy  and  dilatation  of  right  ventricle  and  of  the  left  auricle.  Atheroma  of 
the  aorta. 

Heart:  Weighs  480  gm.  The  right  auricle  is  distended  with  black  blood-clots  and  its 
cavity  is  large.  Its  wall  measures  O.o  cm.  at  its  thickest  portion  and  its  muscle  is  firm. 
The  endocardium  is  opaque  and  presents  reddish  discolorations  in  some  areas.  The  mitral 
orifice  measures  3  cm.  in  diameter.  The  right  ventricle  has  a  separate  apex  and  seems  large; 
its  wall  measures  1  cm.,  its  color  is  bright  red,  and  its  endocardium  is  smooth  and  glistening. 
The  tricuspid  leaflets  show  slight  thickening  along  the  hne  of  contact.  The  pulmonary  valves 
are  incompetent  owing  to  a  perforation  in  the  posterior  leaflet.  The  left  auricle  is  very  large; 
its  muscle,  which  is  firm  and  pale,  measures  5  mm.  Beginning  at  the  mitral  orifice  and  extend- 
ing along  the  posterior  wall  of  the  auricle  is  an  area  4  x  6  cm.,  of  closely  set,  irregidar,  pinkish 
vegetations,  many  of  which  measure  3  mm.  in  height,  and  which  have  somewhat  the  appearance 
of  necrotic  bone.  The  left  ventricle  is  also  large,  has  a  distinct  apex,  and  measures  16  mm.  in 
thickness.  On  the  anterior  surface  of  the  ventricular  endocardium  are  two  irregular  circular 
areas,  one  measuring  6  mm.,  the  other  3  mm.  in  diameter,  consisting  of  elevated  granular, 
pinkish  vegetations.  The  smaller  of  these  is  superficial;  the  larger  extends  almost  to  the 
pericardial  surface.  The  auricular  aspect  of  the  mitral  valve  presents  an  appearance  similar 
to  that  of  the  posterior  wall  of  the  left  auricle.  The  edges  of  the  leaflet  are  comparatively 
smooth,  although  vegetations  are  occasionally  noted.  At  the  junction  of  the  posterior  and 
internal  leaflets  a  perforation  is  seen. 

(Photograph  by  Dr.  A.  R.  Allen.) 


30  STUDIES   IN    CARDIAC    PATHOLOGY 

statistics  this  point  is  certainly  underestimated,  because  of  the 
greater  facilities  for  laboratory  methods  at  the  command  of  the 
clinicians  in  a  modern  hospital.  Blood-cultures  when  carefully 
and  repeatedly  made  are  of  the  greatest  assistance  in  arriving 
at  correct  conclusions. 

Among  107  cases  of  acute  endocarditis  autopsied  at  the  Penn- 
sylvania Hospital  the  endocarditis  was  correctly  diagnosticated 
in  24  instances.  In  many  cases  the  true  condition  was  completely 
overshadowed  by  other  conditions.  The  following  diagnoses 
were  recorded:  typhoid  fever,  12;  pneumonia,  9;  chronic  en- 
docarditis, 14;  septicemia,  3;  chronic  nephritis,  4;  acute  peri- 
carditis, 3;  miliary  tuberculosis,  1;  congenital  heart  disease,  1; 
rheumatic  fever,  1;  renal  calculus,  1;  asthma,  3;  etc.  Nine 
cases  were  admitted  in  a  moribund  condition,  and  no  diagnosis 
established.  These  figures  cast  no  reproach  upon  the  physicians 
of  the  hospital,  who,  as  is  well  known,  stand  in  the  foremost 
rank  of  the  Philadelphia  medical  world.  They  merely  illustrate 
the  insidious  nature  of  the  pathologic  process  which  we  have  been 
discussing.  It  should  also  be  borne  in  mind  that  in  the  vast 
majority  of  these  cases  the  diagnoses  made  were  correct.  The 
endocarditis  was  simply  a  complication  of  other  diseases,  which 
did  not  manifest  itself  b}^  prominent  sj^mptoms  or  physical  signs. 

CHRONIC  INFECTIVE  ENDOCARDITIS 

Bacteriology. — Horder,"^  who  has  been  more  fortunate  than 
most  other  investigators,  states  that  with  careful  technic,  positive 
blood-cultures  can  be  obtained  intra  vitam  sooner  or  later  in 
90  per  cent,  of  all  cases  of  infective  endocarditis.  He  has  published 
analyses  of  40  cases,  in  27  of  which  the  bacteriologic  findings  were 
substantiated  at  autopsy  as  follows:    Streptococcus,  26;  bacillus 

'Details  of  Herder's  technic,  Practitioner,  Nov.,  190.5.  "Treatment  with  Vaccines" 
(Horder),  Practitioner,  1908,  p.  714.  Positive  blood-cultures  in  28  consecutive  cases:  Strep- 
tococcus, IS;  bacillus  influenzie,  5;  pneumococcus,  3;  gonococcus,  1;  staphylococcus,  1. 
Hence  the  streptococcus  type  caused  65  per  cent.,  or,  if  including  pneumococcus,  77  per  cent., 
of  all  cases.     See  also  Libman  and  Celler  (43  cases) :  Trans.  Assoc.  Amer.  Phys.,  May,  1910. 


ACUTE    KNDOCARDITIS  31 

influenzae,  5;    pneumococcus,  5;    gonococcus,  2;    staphylococcus 
albus,  1;   unidentified,  1. 

It  will  be  observed  that  the  genus  streptococcus  causes  77 
per  cent,  of  the  cases  (some  6  cases  in  which  bacillus  influenzae 
was  successfully  cultivated  from  blood  are  now  on  record).  He 
quotes  100  postmortem  cultures  from  the  heart's  blood  as  corrob- 
orating his  intra- vitam  findings. 

Following  surgical  infections  the  staphylococcus  aureus  is 
more  frequent.  These  infections,  which  are  seen  in  osteomyelitis, 
etc.,  are  often  rapidly  fatal.  Differentiation  of  the  varieties 
of  streptococci  based  upon  certain  metabolic  reactions  seems  to 
show  that  the  streptococcus  generally  found  in  endocarditis  is 
not  the  same  species  which  is  found  in  acute  suppurative  conditions. 

Border's  investigations  indicate  that  infective  endocarditis 
is  generally  due  to  streptococci  of  low  virulence,  such  as  those 
normally  found  in  the  saliva  and  the  intestinal  tract,  a  fact  which 
explains  the  jDrotracted  insidious  character  of  this  so  frequently 
overlooked  process.  "It  may  be  that  the  very  lowness  of  the 
virulence  of  these  habitual  saprophytes  of  the  alimentary  canal 
accounts  for  the  lack  of  efficient  resistance  on  the  part  of  the 
patient,  there  being  no  adequate  stimulus  to  call  forth  the  de- 
fensive mechanisms  necessary  for  the  destruction  of  the  cocci" 
(Horder) . 

Horder  suggests  the  following  classification : 
I.  Latent  infective — a  terminal  condition,   in  old  valvular 
cases,  etc. 

II.  Fulminating  infective. 

III.  Acute  infective — the  clinical  picture  is  that  of  pneumonia, 
it  is  often  due  to  pneumococcus. 

IV.  Subacute  infective — the  commonest  variety  associated 
with  a  gradual  development  of  dyspnea,  weakness,  arthritis  or 
chorea,  etc.,  lasting  from  two  to  six  months. 

V.  Chronic  infective:   Insidious — ambulant  cases — organisms 
of  low  virulence — streptococcus  fecalis  often  found. 


32  STUDIES  IN  CARDIAC  PATHOLOGY 

The  valvular  form  of  syphilitic  endocarditis,  except  when  it 
follows  aortitis,  is  generally  secondary  to  syphilitic  myocarditis  as 
the  result  of  direct  extension.  Parietal  lesions  are  more  frequent 
than  valvular  alterations.  Macroscopically  they  often  show  no 
sclerotic  changes.  Occasionally,  however,  as  in  a  case  reported 
by  Duckworth/  minute  gummata  occur.     The  seat  of  predilection 

'  Duckworth:   Lancet,  1895. 


Fig.  10. — Acute  Ulcerative  Mitral  and  Aortic  Endocarditi.s. 

Negro.  (Pennsylvania  Hospital.  Autopsy  No.  328.  Pathologist:  Dr.  Longcope. 
Physician:  Dr.  A.  Stengel.) 

Clinical  Notes:  Twenty-three  years  old.  Denies  venereal  disease.  Has  never  been 
ill  before,  except  with  pneumonia  six  months  ago.  For  the  last  four  days  has  had  dyspnea, 
chills,  and  vomiting. 

Heart  dullness  much  enlarged.  Apex-beat  forcible  and  diffuse.  Systolic  thrill  near  apex. 
Pulmonic  second  sound  accentuated.  A  loud,  long,  diastolic  murmur  over  the  heart,  and 
through  both  sides  of  the  chest. 

Pathologic  Notes:  Acute  ulcerative  mitral  and  aortic  endocarditis.  Acute  myocarditis; 
acute  hemorrhagic  pericarditis,  etc. 

Heart:  is  much  enlarged;  feels  like  thick-walled  cyst,  and  is  rather  rounded  in  shape. 
It  collapses  about  the  hand  when  held  at  the  apex.  Epicardium:  irregular  areas  of  opaque, 
white  thickening  over  surface  of  left  ventricle.  Sometimes  these  follow  the  vessels,  which 
are  otherwise  not  very  prominent.  Beneath  the  endocardium,  heart  has  mottled  yellow 
appearance,  and  shows  numerous  ecchymotic  hemorrhages  at  the  vascular  terminations. 
Tricuspid  and  pulmonary  valves  normal;  the  orifices  measure  respectively  13  and  7.5  cm.  in 
circumference.  Right  ventricle,  4  mm.,  left  ventricle  distended  by  clot.  Left  auricle  slightly 
dilated.  Mitral  valve  is  seat  of  extensive  ulcerative  endocarditis;  the  vegetations,  situated  especially 
on,' the  auricular  surface,  are  yellowish,  soft,  and  friable.  They  frequently  measure  1  cm.  in  diam- 
eter, and  project  high  above  the  valve  surface.  Smaller  vegetations  on  the  surface  of  the  auricle. 
From  the  free  border  of  the  aortic  valves  two  large  pendulous  thrombi  hang  into  the  ventricle, 
measuring  2  cm.  in  length,  the  valve  being  much  ulcerated  at  their  point  of  attachment,  the 
thrombi  covering  the  ulceration.  On  the  endocardium  of  the  ventricle  there  is  a  patch  2  cm.  in 
diameter  below  the  insertion  of  the  aortic  valves,  covered  with  small  yellowish  accumulations. 
Aortic  valves  thickened  and  ulcerated  along  their  free  margins.  Heart-muscle  soft  and  friable, 
pale  brownish-gray.  Sprinkled  through  the  section  are  minute  yellow  points;  one  or  two  large 
ones  (1  to  2  cm.  in  diameter).  Papillary  muscles  and  columnce  carnece  of  both  ventricles  much 
fliUened.  Left  ventricle  1  cm.  Definite  cardiac  contractions  are  elicited  by  pinching  muscle 
with  forceps;  especially  is  this  true  of  the  papillary  muscles  (one  and  three-fourths  hours  after 
d3ath). 

Microscopic  Examination:  Muscular  strise  poorly  marked.  Nuclei:  large,  pale,  in- 
dsSnite,  and  in  some  places  surrounded  by  clear  spaces.  Muscle-cells  show  moderate  frag- 
mentation; many  are  filled  with  large  vacuoles.  Slight  hemorrhages  are  scattered  through 
the  SBction,  beneath  the  endocardium  and  pericardium.  They  are  fairly  extensive.  The 
vacuole-like  degeneration  is  most  marked  near  the  hemorrhages,  and  everywhere  occurs  in 
patches.  At  one  point  a  mass  of  polymorphonuclear  leukocytes  is  seen  in  the  myocardium; 
surrounding  it  there  are  some  hemorrhages  and  much  degeneration  of  muscle-cells.  In  the 
mass  of  muscle  degeneration  the  muscle-nuclei  have  entirely  disappeared. 

Acute  parenchymatous  degeneration  of  the  myocardium. 

The  pneumococcus  was  obtained  from  the  heart's  blood  and  the  vegetations. 


34  STUDIES   IN    CARDIAC    PATHOLOGY 

seems  to  be  the  left  ventricle.  When  the  valves  are  attacked, 
the  lesions  are  often  limited  to  a  valve  or  part  of  a  valve.  Sclerotic 
changes — retraction,  etc. — ultimately  result.  Taneff^  collected 
95  cases  of  syphilitic  endocarditis,  in  10  of  which,  however,  the 
etiologic  factor  was  questionable.-  (Compare  chapters  on  aortic 
endocarditis  and  cardiac  syphilis.) 

Trauma  may  produce  valvular  lesions  in  two  ways:  Either 
(a)  by  rupture  of  a  papillary  muscle  or  chorda  tendinese,  or 
(6)  by  rupture  of  the  endocardium,  with  the  production  of  thrombi 
or  subendothelial  hemorrhages.  Injuries  which  produce  such 
valvular  damage  generally  consist  of  crushing  forces  or  violent 
blows.  It  is  verj^  doubtful  whether  mere  sudden  increase  in 
vascular  tension  as  a  result  of  heavy  lifting,  etc.,  is  capable  of 
rupturing  an}"  part  of  a  healthy  heart.  Such  cases  are  reported, 
but  are  presumably  the  result  of  localized  weakening  through 
antecedent  pathologic  processes.     Blows  inflicted  in  the  precordial 

'  Inaug.  Dissert.,  Berlin,  1896. 

-Complete  literature  by  Herxheimer:  Lubarsch  and  Ostertag's  Ergebnisse  der  allg. 
Path.,  i,  1906. 

Fig.  11. — Acute  Vegetative  and  Chronic  Endocarditis. 

W.  R.,  male,  aged  forty-six  years.  (Pennsylvania  Hospital.  Autopsy  1165.  Physician: 
Dr.  J.  A.  Scott.     Pathologist:   Dr.  Krumbhaar.) 

Clinical  Notes:  The  patient,  who  is  an  alcoholic,  has  been  ill  for  two  days  with  cough 
and  chills.  Lungs:  full  of  rales.  An  apparent  pulmonary  consolidation  at  the  left  base. 
Cyanosis,  tremors.  Heart  negative.  Death  two  days  later,  suddenly,  apparently  from  acute 
cardiac  dilatation. 

Pathologic  Diagnosis.  Lobar  pneumonia.  Acute  vegetative  and  chronic  endocarditis. 
Pulmonary  congestion  and  edema. 

Pericardium:  Contains  30  c.c.  of  turbid  yellow  fluid,  with  a  few  fibrinous  flakes. 

Heart:  The  heart  is  much  enlarged  (490  grams),  especially  to  the  right.  It  is  greatly 
distended  with  currant-jelly  and  pinkish  chicken-fat  clots.  Except  for  a  patch  of  thickening 
on  the  posterior  surface,  the  epioardium  is  negative.  The  mitral  orifice  admits  three  fingers. 
Tlieh-fl  nnlrirtc  is  enlarged,  and  measures  from  1 ',  In  IS  mm.:  it  is  somewhat  pale  and  friable. 
The  iniliiiMrdium  is  smooth.  All  three  aorlir  i-iisp.':  .ilmir  mnrkedly  a  vegetative  growth.  The 
cusp  opposite  the  right  coronary  artery  shows  tlic  :;iiiiillisl  rvijcldlton,  which  is  limited  to  the  cardiac 
side  of  the  valve.  The  growth  is  yellomsh,  irregular,  nodular,  and  in  some  places  calcareous,  the 
greater  part,  however,  being  semitransparent,  soft,  and  friable.  The  vegetations  on  the  other  valves 
are  soft  and  gray.  They  are  irregularly  nodular  with  a  finely  granular  surface.  One  of  them, 
measures  1  cm.,  the  other  2.5  cm.  in  length.  The  large  vegetation  has  a  base  about  1  cm.  in  breadth, 
so  that  it  is  freely  movable  in  the  left  ventricular  cavity.  The  mitral  valve  shows  slight  thickening. 
The  aortic  cusp  at  the  highest  point  of  its  attachment  shows  a  similar  thickening.  The  coronary 
arteries  are  large,  thin,  and  patent.  The  valvular  orifices  measure  as  follows:  Tricuspid,  12  cm.; 
mitral,  12  cm.;  pulmonary,  S  cm.;  aortic,  8.5  cm. 


36  STUDIES  IN  CARDIAC  PATHOLOGY 

region  may  produce  endocardial,  pericardial,  or  myocardial  lesions, 
even  when  the  skin  and  thorax  remain  uninjured.  Among  34 
animals  experimentally  studied  by  Kuelbs^  the  following  lesions 
were  produced:  valvular  damage,  21;  distributed — mitral  12, 
aortic  7,  tricuspid  5,  pulmonic  4.  All  of  these  lesions  were  hem- 
orrhagic. Actual  valvular  rupture  occurred  once.  In  no  instance 
were  any  of  the  chordse  tendinese  torn.  Mj^ocardial  damage 
followed  in  15  cases  and  consisted  chiefly  of  hemorrhages  or  tears 
in  the  septum.  In  one  case  there  was  cardiac  rupture.  The 
pericardial  lesions  were  eleven  in  number,  mainly  hemorrhagic  in 
character.  None  of  the  cases  showed  loss  of  compensation,  and 
onl}^  rarely  were  murmurs  present.  Experimental  valvular  lesions 
in  animals  show  a  very  marked  tendenc}'  to  rapid  healing  with 
simple  scar  tissue  formations.^     If  there  is  a  chance  for  infection, 

'  Kuelbs:  Mitt.  a.  d.  Grenz.  der  Med.  u.  Chir.,  1909,  p.  679. 

-  For  trauma  as  a  cause  of  endocarditis,  etc.,  see :  Stern,  Ueber  die  traumatische  Entstehung 
innerer  Krankheiten,  vol.  i;  Thorel,  Lubarsch  and  Ostertag's  Ergebnisse,  1907,  ii,  434;  Drey- 
fuss,  These  de  Paris,  1896;  Heimann,  Dissert.  Berlin,  1896;  Sinnuber,  Deut.  med.  Woch., 
1904,  No.  32;  Frankel,  Miinch.  med.  Woch.,  1905,  No.  15;  Marcus,  ibid.,  No.  47;  Herzfeld, 
Jour.  Am.  Med.  Assoc,  1906,  p.  855. 


Fig.  12. — Ulcer.\tive  Aortic  Endocarditis. 

I.  S.,  male,  white,  aged  forty-eight  years.  (Pennsylvania  Hospital.  No.  320  (1902). 
Autopsy  189.     Pathologist:  Dr.  Longoope.) 

Pathologic  Diagnosis:  Ulcerative  aortic  endocarditis.  Globular  throinbus  attached  to 
aortic  value.  Extensive  multiple  thrombosis  of  arteries  and  veins.  Acute  bronchopneumonia. 
Chronic  pulmonary  tuberculosis,  etc. 

Heart:  The  heart  is  quite  small,  weighs  250  grams.  The  epicardium  contains  a  moderate 
amount  of  fat  and  two  milk  patches.  The  tricuspid,  pulmonary,  and  mitral  valves  are  normal. 
The  left  ventricle  is  very  small,  measuring  only  7  cm.  from  the  aortic  valve  to  the  tip;  it  is  15 
mm.  in  thickness.  On  the  mitral  cusp  of  the  aortic  valve  is  a  large  globular  thrombus  which  meas- 
ures 2  cm,,  in  diameter,  being  firmly  attached  to  the  outer  portion  of  the  valve.  It  projects  into  the 
aortic  orifice,  forming  as  it  were  a  complete  plug  for  it,  when  the  valves  are  in  normal  position. 
It  is  mixed  red  and  gray  in  color,  somewhat  tabulated  and  firm.  The  sinus  of  Valsalva  of  the 
valve  is  filled  with  a  recent  thrombus  of  similar  character  which  projects  about  8  mm.  above  the  velum 
of  the  valve.  The  two  globidar  thrombi  are  joined  by  a  fibrinous  band.  The  portions  of  the  leaflet 
which  are  uninvolved  are  thin  and  delicate,  as  is  also  the  velum.  The  other  two  valve  cusps 
are  a  trifle  thickened,  but  still  delicate  and  evidently  competent.  The  heart  muscle  is  brown 
and  firm;  and  the  endocardium  is  slightly  flecked  with  yellow.  The  aorta  is  small.  The 
coronaries  are  patent. 

Microscopically  the  thrombi  consist  largely  of  erythrocytes  and  fibrin: 

Bacteriologic  Diagnosis:  Heart's  blood:  Sterile  after  forty-eight  hours  at  36.5°  C. 
Thrombi  on  aortic  valve :  Streptococcus  pyogenes.  Lung:  Micrococcus  lanceolatus.  Throm- 
bus from  vena  cava;  Bacillus  coli. 


38  STUDIES  IN  CARDIAC  PATHOLOGY 

however,  as  when  the  animals  are  kept  in  dirty  kennels,  these 
injured  valves  not  infrequently  become  the  seat  of  an  acute 
endocarditis. 

A  considerable  number  of  instances  of  traumatic  valvular 
disease  have  been  recorded,  as,  for  instance,  a  case  of  Schmidt's^ 
of  an  aged  patient  falling  out  of  a  second-story  window  and  rup- 
turing the  aortic  and  mitral  valves. 

The  danger  of  trauma,  then,  in  relation  to  endocarditis  is 
twofold.  It  may  reactivate  a  quiescent  lesion,  or  it  may  prepare 
the  soil  of  a  previously  healthy  endocardium  for  subsequent  in- 
fection. Its  action  may  be  direct,  through  the  force  of  a  blow, 
or  indirect,  as  the  result  of  suddenly  increased  blood-pressure. 

The  endocardial  changes  following  infectious  endocarditis  are 
in  some  respects  different  from  those  due  to  purely  mechanical 
causes,  as  in  chronic  valvular  disease.  Thus,  for  instance,  in 
the  latter  case  the  line  of  valvular  closure  of  the  leaflets  shows  the 
principal  changes;    in  the  former,  the  free  margins  are  involved. 

'  Schmidt:  Miinoh.  med.  Wooh.,  Sept.  23,  1902.  Claisse  and  Socquet  report  the  case  of  a 
healthy  man  of  forty-eight  years  who  was  crushed  on  the  chest  by  a  heavy  stone  which  he  was 
trying  to  lift  into  place.  The  injury  was  followed  by  sudden  pain  and  dyspnea.  At  autopsy 
five  months  later  a  ruptured  papillary  muscle  was  found.  (Bull,  et  Mem.  Soc.  M6d.  des  Hop. 
de  Paris,  1908,  p.  769.)  Another  case  was  reported  by  Marcus.  (Mlinch.  med.  Woch.,  1905, 
p.  228). 


11.  CHRONIC  ENDOCARDITIS 

The  term  "chronic  endocarditis"  as  currently  applied  is 
ambiguous.  It  should,  of  course,  be  limited  to  those  cases  in 
which  an  acute  endocarditis  has  become  established  as  a  continuous 
progressive  process;  but  often  it  is  employed  to  designate  an 
old  endocardial  lesion,  even  of  the  arteriosclerotic  type,  the  course 
of  which  may  have  been  completely  arrested.  On  the  other  hand, 
we  must  bear  in  mind  that  in  many  apparently  quiescent  cases 
active  inflammation  due  to  organisms  of  low  virulence  or  the 
fibrogenic  activities  of  an  antecedent  inflammation  may  still  be 
operative. 

The  term  chronic  endocarditis  is  generally  applied  to  a  fibrotic 
process  which  follows  an  acute  infection.  About  one-half  of  the 
cases  of  valvular  heart  disease  arise  in  this  manner,  the  remainder, 
with  negligible  exceptions,  resulting  from  the  arteriosclerotic 
changes  of  advancing  life.  As  in  other  parts  of  the  body,  destruc- 
tion of  tissue  is  followed  by  the  formation  of  scars,  which  on  the 
endocardium  produce  deformities  of  the  valves  and  their  orifices 
by  contraction,  induration,  puckering,  and  adhesion,  and  ulti- 
mately in  some  cases  calcification.  In  this  manner  valvular 
obstruction  and  insufficiency  may  be  developed. 

In  the  mitral  area  the  occurrence  of  adhesions  tends  to  fuse 
together  the  valvular  curtains,  and  if  the  chordse  tendinese  are  also 
involved,  a  funnel-shaped  orifice  results.  Skrinking  and  fibrosis 
continue,  thus  bringing  about  more  and  more  induration,  shorten- 
ing, and  stiffening.  If  only  partial  union  of  the  free  lateral  valve 
margins  occurs,  a  sfit-like  opening  is  left — the  "buttonhole  mitral." 
The  anterior  flap  of  the  mitral  is  most  frequently  and  extensively 
involved,  especially  in  the  region  nearest  to  the  aortic  valve, 
where  the  greatest  strain  occurs  owing  to  the  auriculo-ventricular 
and   the   vontriculo-aortic  blood-stream.     Organic  mitral  disease 


40  STUDIES  IN  CARDIAC  PATHOLOGY 

generally  follows  infectious  endocarditis,  while,  excepting  syphilis, 
aortic  lesions  are  more  often  the  result  of  arteriosclerosis.  Mitral 
stenosis  also  is  verj^  commonly  a  sequel  of  endocarditis;  pure 
insufficiency  is  less  often.  Contraction  and  induration  result 
from  the  organization  of  granulation  tissue,  and  in  this  process 
the  chordse  tendinese  and  the  papillary  muscles  often  share. 
Calcification  which  results  from  the  deposition  of  lime  salts  in  the 
diseased  areas  produces  roughness  and  inflexibility.  In  this  process 
the  aortic  valves,  especially  about  the  corpora  Arantii  and  along 
the  free  margins,  are  chiefly  affected.  In  all  cases  of  valvular 
damage  the  amount  of  calcium  ions  in  the  blood  plays  an  important 
part  in  the  degree  and  extent  of  the  lesions  produced.  This 
process  of  calcification  is  nature's  method  of  repairing  weak  spots 
and  leaks,  and  in  robust  plethoric  individuals  she  often  overplays 
her  part.  As  Sir  James  Barr  puts  it  in  speaking  of  the  calcium 
ions  in  relation  to  mitral  stenosis:  "They  raise  blood-pressure, 
increase  the  force  of  the  cardiac  contractions,  give  rise  to  hyper- 
trophy of  the  papillary  muscles,  cause  violent  collision  of  the 
mitral  cusps,  increase  the  formation  of  fibrous  tissue,  and  gradually 
cement  and  unite  the  edges  of  the  cusps  together." 

In  sclerotic  endocarditis  not  only  the  valvular  leaflets,  but 
also   the   chordse   tendinese   and   papillary   muscles   are   affected. 


Fig.  13. — Acute  Vegetative  and  Ulcerative  Aortic  and  Mitral  Endocarditis. 

W.  G.,  male,  aged  fifty-six  years.  (Philadelphia  Hospital,  vol.  xviii,  p.  142.  Physician: 
Dr.  R.  G.  Curtin.     Pathologist:  Dr.  Guthrie  McConnell.) 

Clinical  Notes:  A  paroxysmal  drunkard;  was  admitted  with  cough,  edema,  and  dysp- 
nea. 

Physical  Examination. — Heart  is  enlarged  to  right  and  left.  A  systolic  murmur  is 
heard  at  the  apex  and  transmitted  to  the  axilla.  A  doubtful  systolic  murmur  is  heard  at  the 
aortic  area.  The  second  sounds  at  the  base  are  indistinct.  The  patient  developed  uremic 
symptoms  and  died  suddenly  during  an  attack  of  coughing  associated  with  marked  cyanosis. 

Pathologic  Diagnosis:  Acute  vegetative  and  xdcerativc  aortic  and  mitral  endocarditis. 
Cardiac  hypertrophy,  hydrothorax,  ascites,  chronic  parenchymatous  nephritis,  etc. 

Heart:  Weighs  620  gm.  The  middle  leaflet  of  the  aortic  valve  shows  a  vegetation  13  x  10x3 
mm.,  soft  in  consistence,  reddish-yellow  in  color.  Smaller  vegetations  are  seen  on  the  other  leaflets 
and  on  the  mitral  valve,  the  anterior  curtain  of  which  shoxvs  a  circular  ulcerated  area,  10  mm.  in 
diameter,  the  central  portion  of  which  has  completely  perforated  the  leaflet.  The  auricular  surface 
is  covered  by  a  large  irregular  vegetation.  The  chorda;  tendinece  show  many  pinhead-sized 
vegetations.     The  pulmonary  valves  are  normal.     The  tricuspid  orifice  is  dilated. 


42  STUDIES   IN    CARDIAC    PATHOLOGY 

Lowenstein^  in  a  study  of  the  fibrosis  of  the  latter  was  led  to  con- 
clude that  these  fibroid  changes  are  secondary  to  previous  muscular 
degeneration,  a  process  to  which  this  part  of  the  cardiac  muscula- 
ture seems  to  be  especially  susceptible.  Actual  bone  formation 
in  the  valves  and  even  the  heart  itself  has  been  described. 

Frequency. — The  frequency  of  valvular  disease  and  the  type 
vary  considerably  in  different  statistics,  at  different  ages,  in  the 
two  sexes,  and  according  to  the  etiologic  factor.  Thus,  under 
forty  years  of  age,  especially  in  women  and  in  children,  and  as 
the  result  of  rheumatic  endocarditis,  mitral  lesions  are  in  pre- 
ponderance. After  forty  years  of  age,  and  in  men  (especially 
syphilitics  and  arteriosclerotics),  aortic  lesions  assume  the  pre- 
dominating role.  Andrew  among  1,474  cases  of  heart  disease 
found  887  (60.1  per  cent.)  in  men,  and  587  (39.8  per  cent.)  in 
women.  Endocardial  lesions — acute  and  chronic — formed  87 
per  cent,  of  the  total  number  of  cardiac  ailments  (pericardial 
5.4  per  cent.,  myocardial  5.5  per  cent.).  The  greatest  number  of 
chronic  mitral  cases  occurred  between  twenty  and  thirty  years, 
of  aortic  disease  between  forty  and  fifty  years,  and  degenerative 
myocardial  changes  after  fifty  years.-  The  statistics  of  Bollinger 
and  of  Eulenburg  show  that  well-marked  disease  of  the  cardiac 
valves  or  orifices  occurs  in  from  5  to  10  per  cent,  of  all  autopsies. 

From  a  morphologic  standpoint  Dewitsky^  has  formulated  the 
five  following  types  of  chronic  valvular  lesions: 

I.  Diffuse  infiltration  of  the  leaflets:  an  extension  from  the 
endocardium,  inflammatory  in  character,  the  terminal  phase  of 
an  acute  endocarditis. 

II.  Lesions  on  the  valvular  edges:  resulting  from  hyper- 
trophy of  the  subendothehal  layer,  caused  by  relative  insufficiency 
of  the  valves  affected. 

III.  Lesions  at  the  base  of  the  leaflets:  a  quasi-physiologic 
process  found  with  increasing  frequency  as  life  advances. 

^  Lowenstein:  Centralb.  f.  allg.  Path.  u.  path.  Anat.,  1907,  p.  385. 

^Andrew:   "Age  Incidence,  Sex  and  Comparative  Frequence  of  Disease,"  London,  1909. 

'  Dewitsliy:  These  du  Mo.scow,  1908.     (See  also  Virchow's  Archiv,  1910,  excix.) 


CHRONIC    ENDOCARDITIS 


43 


IV.  Lesions  found  only  on  semilunar  valves:    arteriosclerotic 

in  nature  and  extending  from  the  vascular  wall  to  the  leaflets. 
V.  Lesions  on  the  free  border  of  the  aortic  valve:    resulting 

from    thrombotic    changes    initiated    by    an    acute    endocarditis 

(infectious). 

(These  types,  though  distinct,  are  often  mixed.) 

From  a  clinical  standpoint  the  relative  involvement  of  different 

valves  has  been  reported  as  follows : 


Ashton  (Med.  News,  June  .30, 

1894) 

Crook  (N.  Y.  Med.  Jour.,  1897, 

821). 

Satterthwaite  (Dis.  of  Heart  and 

Aorta) 

Chambers    (Med.    Times   and 

Gazette,  1852) 

Bamberger  (Virchow's  Arch.,  ix, 

p.  524) 

Schnitt  (Dissert.  Jena.,  189-3) .  . 
Leuch  (Dissert.  Zurich,  1889) .  . 
Hirsch,  (Mitt.  a.  d.  Med.  Khnik, 

Wurtzb  ,  vol.  ii,  p.  305)  .  .  . 
Koster     (Dissert.     Gottingem, 

1883) 

Leuch  67 

Guttmann     (Dissert.     Breslau 

1891) 13961 

SperHng  (quoted  Gibson) i  300 

Middleton  (Lancet,  1889) . 

Sansom \  300 

Lambert  (J.  A.  M.  A.,  1908)  .  .  . .  i  283 

Olsen 

Pennsylvania  Hospital  (autop-  1 

sies) !  274 


1024 

478 

65 

367 

211 
210 
241 

203 


116i 


63 

7 

13 

13 

934 

283 

1.57i  40 

801  20 

255!  129 

2.32  124 

29 1  26 

84 

114 

3226 

1315 

gf^ 


4     12      5S 
116     68    691 


A  valvular  aneurism  consists  of  a   "circumscribed  pouching 
(jf  onf  of  the  valve  segments."     Two  varieties  are  met  with: 

(a)  In  which  the  whole  thickness  of  the  leaf  is  pouched. 

(b)  In  which  as  the  result  of  ulcerative  endocarditis  the  lamellae 
of  tlic  valves  have  become  dissected  apart. 


44  STUDIES   IN    CARDIAC    PATHOLOGY 

Valvular  aneurisms  vary  in  size  from  a  small  lentil  to  a  small 
pigeon's  egg,  and  are  occasionally  multiple.  The  mitral  valve 
is  most  frequently  attacked  and  shows  the  largest  aneurisms, 
although  rupture  occurs  more  frequently  when  the  aortic  valves 
are  involved.  In  some  chronic  cases,  instead  of  rupture, thrombosis 
of  the  sac  occurs.     (See  Fig.  14.) 

Clinical  Considerations. — Given  a  case  of  valvular  heart 
disease,  the  practitioner  is  called  upon  to  determine  a  number  of 
questions:  The  site  of  the  lesion,  whether  it  is  obstructive,  or 
regurgitant,  or  combined;  whether  more  than  one  valve  is  in- 
volved. What  is  the  severity  of  the  lesion  as  regards  actual 
mechanical  effects?  What  is  the  cause  of  the  lesion — infectious, 
arteriosclerotic,  or  merely  functional?  Is  it  apt  to  be  progressive? 
and  if  so,  how  rapidly?  Is  the  actual  infection  still  continuing? 
The  importance  of  the  last  question  cannot  be  overestimated, 
and  it  is  bj'  no  means  easily  answered.  As  has  already  been 
stated,  the  infection  often  goes  on  insidiously  for  months.  Thacher 
has  called  attention  to  the  persistence  of  fever  in  many  of  these 
cases,  and  Coleman  has  pointed  out  how  exactly  the  fever  curves 
may  simulate  different  tjqoes  of  malarial  infection.^  With  the 
possible  exception  of  the  last  question  the  following  is  the  most 
important  of  all:  What  is  the  state  of  the  mj'ocardium, — how 
much  actual  damage  has  it  sustained,  either  from  the  infection 
or  from  the  degenerative  changes  of  age,  syphilis,  tobacco,  etc.? 
The  French  have  an  axiom  which  well  emphasizes  this :  "A  disease 
of  the  valves  is  not  a  disease  of  the  heart." 

As  to  the  duration  of  life,  this  of  course  varies  greatl.y.  In 
Romberg's  clinic  one  patient  was  known  to  have  lived  thirty-eight 
years  with  a  valvular  lesion.  Sir  Andrew  Clark  in  a  study  of 
700  cases  found  that  often  there  was  practically  no  shortening 
of  life.  The  emergencies  of  life  and  infectious  processes  are  less 
well  withstood. 

When  cardiac  failure  does  occur,  it  is  hj  no  means  rarely  due 

'  Amer.  ,Jour.  Mod.  Sci.,  March,  190.5. 


Fig.  14, — Large  Aneurism  of  the  Mitral  Valve  with  Fenestration. 

Bulging   into   the  auricular   cavity.    (Specimen   from   tlie   University  of   Pennsylvania 

Museum.) 


46  STUDIES  IN  CARDIAC  PATHOLOGY 

to  chronic  infection,  at  least  this  is  Stein's^  conclusion,  and  this  is 
borne  out  by  the  results  of  artificially  produced  valvular  lesions 
in  animals. 

While  combined  valvular  lesions  are  often  doubly  disad- 
vantageous, they  may  to  a  certain  extent  be  beneficial  and  com- 
pensating. Thus  an  aortic  obstruction  added  to  an  insufficiency 
may  to  some  extent  prevent  left  ventricular  dilatation;  the 
mitral  insufficiency  which  is  sometimes  engrafted  upon  an  ob- 
struction represents  a  certain  grade  of  healing  (Krehl) . 

Heredity. — A  hereditary  tendency  to  certain  forms  of  heart 
disease  seems  to  exist.  Perhaps  the  best  known  type  is  that 
described  by  Huchard  as  "aortism,"  by  which  is  meant  the  well- 
known  plethoric,  hypertensive,  ultimately  arteriosclerotic  type 
of  man  who  dies  suddenly  of  apoplexy,  and  in  whose  family  this 
history  is  very  common. 

The  term  "myocardism"  has  been  suggested  by  Galli  for 
the  type  of  individual  in  whose  familj^,  although  demonstrable 
arteriosclerosis  is  not  a  prominent  feature,  there  is  a  tendency 
toward  myocardial  weakness  and  degeneration.'-  Virchow  and 
Beneke  pointed  out  that  a  small  arterial  system  predisposed  to  in- 
fectious endocarditis. 

The  term  "mitralism"  has  also  been  suggested  as  descriptive 
of  a  tendency  to  lesions,  more  especially  stenosis  of  this  orifice. 

STATISTICAL  DATA  FROM  THE  PENNSYLVANIA  AND  THE  PHILADELPHIA 

GENERAL  HOSPITALS 
I.  Endocardium. 

-_.       ,  T-   T  Pennsylvania     Philadelphia 

Mitral  Valve.  Hospital.  Hospital. 


Acute  simple  endocarditis  of  mitral  alone 

Acute  vegetative  endocarditis  of  mitral  alone : \   47 


58 

Acute  ulcerative  endocarditis  of  mitral  alone J  J 

Acute  mitral  and  aortic  endocarditis 23  33 

Acute  mitral  and  tricuspid  endocarditis 2  4 

Acute  mitral,  tricuspid,  and  aortic  endocarditis 2  0 

Aneurism  of  mitral  valve  (with  rupture) 0  1 

Anomaly  of  mitral  valve  (1  fenestration,  1  pouching,  1  su- 
pernumerary leaflets) 0  3 

[Table  continued  on  p.  48.) 

'  Stein:  Nordschr,  Med.  Arch.,  190.5,  xlii.  ■  Galli:  Berlin,  klin.  Woch.,  1907,  p.  372. 


Fig.  15. — Chronic  Mitral  .\nd  Thictjspid  Endocarditis. 

B.  S.,  female,  negro,  aged  twenty-one  years.  (Philadelphia  Hospital.  Autopsy  vol.  xviii, 
p.  1.54.     Physician:  Dr.  Hughes.     Pathologist:  Dr.  McConnell.) 

Clinical  Notes:  Acute  rhewnatic  fever  ionr  years  a.go,  and  again  two  years  ago.  Severe 
leukorrhea  for  last  four  years.  Denies  syphilis,  but  shows  what  are  apparently  luetic  scars. 
Alcohol  moderately.  Four  years  ago  began  to  have  vertigo  and  d3'spnea,  which  have  grad- 
ually increased  in  frequency  and  intensity,  and  were  generally  induced  by  exertion.  For  last 
few  months  has  also  had  cough,  gastric  symptoms,  and  muscae  volitantes. 

Heart  dullness  enlarged.  Presystolic  thrill  within  the  apex,  at  which  area  a  double  mitral 
murmur  is  heard.  Both  second  sounds  are  accentuated,  especially  the  pulmonic.  Pulse  110. 
Death  occurred  gradually  from  pulmonary  congestion. 

Pathologic  Diagnosis:  Chronic  mitral  and  tricuspid  endocarditis;  chronic  pleuritis; 
right-sided  hydrothorax;  congestion  and  edema  of  right  lung;  bilateral  pulmonary  infarction; 
diffuse  nephritis. 

The  pericardium  contains  a  small  amount  of  fluid. 

Heart:  weighs  340  gm.  Aortic  leaflets,  thin  and  transparent.  Mitral  orifice  barely 
tulmils  lip  of  index-finger;  its  leaflets  are  much  thickened.  The  lips  of  the  papillary  muscles  show 
marked  fibrosis.  Pulmonary  leaflets  normal.  Tricuspid  orifice  (the  lowermost  on  plate)  i.s 
small;  leaflets  thickened,  and  on  free  edges  are  numerous  vegetations.  On  one  leaflet  there  is  a 
vegetation  one  inch  in  height,  which  extends  directly  into  the  opening. 


48 


STUDIES    IN    CARDIAC    PATHOLOGY 


Statistical    Data   from  the   Pennsylvania   and  the   Philadelphia   General   Hospi- 
tals— {Continued) 

I.  Endocardium.     Mitral  Valve— (Continued).  "^'hosJitYl'""    ^  HotpfT™''* 

Hematoma  of  mitral  valve 1  1 

Calcification  of  mitral  valve 112 

Stenosis  of  mitral  valve 72 

Rupture  of  mitral  valve 0  1 

Aortic  Valve. 

Acute  vegetative  endocarditis  of  aortic  alone \  o-  -sn 

Acute  ulcerative  endocarditis  of  aortic  alone J 

Acute  aortic  and  tricuspid  endocarditis 0  0 

Acute  aortic  and  pulmonary  endocarditis 0  3 

Aortic  stenosis 6  42 

Aortic  fenestration 2  43 

Aortic  calcification  (ossification) 1  1 

Aortic  anomaly  (bicuspid  valve) 2  3 

Aortic  valvular  aneurism  (with  rupture) 0  1 

Acute  endocarditis  of  all  valves 2  16 

Subendocardial  hemorrhage 13 

Subendocardial  cyst 1  1 

Tricuspid  Valve. 

Acute  vegetative  endocarditis  of  tricuspid  alone \  „  ^_ 

Acute  ulcerative  endocarditis  of  tricuspid  alone > 

Subacute  endocarditis  of  tricuspid 2  0 

Anomaly  (pouching) 0  1 

Supernumerary  leaflets 0  1 

Fenestration 0  1 

Pulmonary  Valve. 
Acute  vegetative  endocarditis  of  pulmonary  valve  alone .  .  .  "1      ^ 
Acute  ulcerative  endocarditis  of  pulmonary  valve  alone  .  .  .  I 

Chronic  pulmonary  endocarditis — sclerosis 1  44 

Congenital  malformation  of 1  4 

Fenestration 0  17 

Supernumerary  leaflets 1  9 

Acute  Mural  Endocarditis. 

(a)  Vegetative \  r,  5 

(b)  Ulcerative ^  "  6 

Auricular  thrombosis \  ^^  '^^ 

Ventricular  thrombosis > 

Tuberculous  endocarditis 0  2 

II.  Myocardium. 

Rupture  of  left  ventricle 0  1 

Rupture  of  left  auricle 0  2 

Rupture  of  right  ventricle 1  0 

Rupture  of 'papillary  muscle,  or  chordse  tendinete 1  1 

Hemorrhage  into  myocardium 4 

Acute  hemorrhagic  myocarditis 2 

Acute  suppurative  myocarditis 1  5 

Sarcoma  of  myocardium 1  4 

Carcinoma  of  myocardium 0  4 


CHRONIC    ENDOCARDITIS  49 

Statistical   Data  from  the   Pennsylvania  and  the   Philadelphia    General   Hospi- 
tals— (Continued) 

nTLjr  ,  ,      ( ri      f        j\  Pennsylvania     Philadelphia 

.    Myocardium— (Conimued).  Hospital.  Hospital. 

Tuberculosis  of  myocardium 1  4 

Gumma  ot  myocardium 2  1 

Cardiac  aneurism 6  3 

Calcification  of  myocardium 0  2 

Infarction  of  myocardium 2  6 

Parietal  thrombus  left  ventricle 7 

Parietal  thrombus  right  ventricle 7 

Tuberculosis  of  aorta ,1  0 

Intenentrictilar  Septum. 

Ulceration  of  interventricular  septum 1 

Perforation  of  interventricular  septum 2  3 

Aneurism  of  interventricular  septum 0  1 

Rupture  of  interventricular  septum 0  1 

Patulous  interventricular  septum 4  1 

Patent  ductus  arteriosus 1  9 

Pennsylvania  Hospital 1300  autopsies 

Philadelphia  Hospital S640  autopsies 

The  foregoing  statistics  were  collected  from  the  autopsy 
records  of  the  two  above  named  hospitals.  The  discrepancy  of 
some  of  the  figures  when  the  two  sources  of  data  are  compared  is 
largely  due  to  the  fact  that  at  the  Pennsylvania  Hospital  only 
acute  cases  are  admitted,  whereas  the  Philadelphia  Hospital, 
being  connected  with  the  almshouse  and  the  insane  asylum,  is 
filled  mainly  with  people  advanced  in  life. 


III.  DISEASES  OF  THE  AORTIC  ORIFICE 

Chronic  aortic  endocarditis  may  be  divided  into  two  classes: 
(a)  cases  secondary  to  infectious  endocarditis,  and  (b)  cases  due 
to  arteriosclerotic  processes.  Calcareous  change,  which  is  nature's 
method  of  repairing  weak  structures,  may  occur  in  either,  but  is 
much  more  marked  in  the  latter  and  in  those  cases  in  which  the 
valvular  disease  has  extended  downward  from  the  aorta.  There 
is,  however,  another  type  of  the  sclerotic  variety  which  is  met 
with  in  middle  life,  which  is  secondary  to  syphilitic  aortitis,  is 
productive  of  valvular  insufficiency,  and  is  less  prone  to  calcareous 
changes. 

Fisher^  calls  attention  to  two  distinct  types  of  aortic  disease: 
one  of  fatty  degeneration  with  subsequent  deposition  of  calcium 
salts,  and  one  in  which  areas  of  grayish  instead  of  yellowish 
thickening  are  found,  the  summits  of  which  may  be  streaked  with 
white  or  yellow,  and  which  are  localized  to  certain  parts  of  the 
arterial  wall. 

AORTIC  OBSTRUCTION 

Occurrence  and  Pathogenesis. — Aortic  obstruction  is  some- 
times a  congenital  lesion,  but  generally  it  results  from  infective 
endocarditis.  It  may  also  be  caused  by  arteriosclerotic  processes. 
In  its  pure  form  it  is  a  distinctly  rare  variety  of  valvular  lesion. 
Syphilis,  so  often  the  cause  of  aortic  insufficiency,  causes  obstruc- 
tion less  often,  since  the  aortitis  which  this  disease  produces  is 
generally  most  marked  about  13^  inches  above  the  valves,  and 
hence  is  more  apt  to  produce  dilatation  and  contractive  shortening 
than  actual  obstruction.  (See  Fig.  71.)  When  aortic  obstruction 
results  from  rheumatic  fever,  the  mitral  valve  is  generally  involved 
also.  The  fact  that  this  combination  is  so  much  commoner  in 
men  than  in  women  would  indicate  that  there  is  some  other  factor, 

1  Fisher:  Hospital,  Mar.  9,  1907,  p.  406. 
50 


DISEASES    OF   THE    AORTIC    ORIFICE  51 

possibly  strain,  concerned.  AUbutt  states  that  the  combined 
lesion  is  commoner  in  women  who  have  had  laborious  occupations. 
Chorea  as  a  cause  of  aortic  obstruction  is  not  frequent.  Gowers  ^ 
in  250  cases  of  chorea  reported  only  three  cases  of  aortic  disease, 
only  one  of  which  was  obstruction. 

Morbid  Anatomy. — The  morbid  anatomy  of  this  condition 
varies  considerably.  Vegetations,  fusion  of  the  leaflets,  infiltra- 
tion, and  stiffening  or  actual  calcification  may  occur.  At  other 
times  the  cause  of  the  obstruction  is  found  in  a  mediastinal  neoplasm 
or  aneurism.  Although  at  first  sight  the  character  of  this  lesion 
would  seem  to  be  one  of  exceptional  severity,  yet  as  a  matter 
of  fact  its  subjects  often  live  a  long  time.  AUbutt-  states  that 
under  favorable  circumstances  life  may  continue  until  the  aortic 
orifice — which  measures  20  mm.  at  birth,  60  mm.  in  adult  hfe, 
and  68  to  70  mm.  in  advanced  years — is  reduced  to  the  size  of  a 
crow-quill  or  less.  He  quotes  Bradbury's  case,  in  which  "the 
chink  by  which  the  blood  found  access  to  the  aorta  was  only  dis- 
covered on  the  closest  search  after  death."  Inasmuch  as  many 
cases  are  prolonged  in  duration  and  progressive  in  character, 
great  hypertrophy  of  the  ventricle  is  often  found.  It  is  in  this 
variet}^  of  valvular  lesion  that  the  so-called  "concentric  hyper- 
trophy" is  most  nearly  approximated.  Practically,  however, 
some  degree  of  dilatation  is  always  associated. 

Rarely  a  double  obstruction  is  found,  one  at  the  aortic  ring 
itself,  and  one  beneath  it,  due  to  sclerosis  of  the  tissue  between 
the  septum  and  the  anterior  mitral  leaflet. 

Coarction  of  the  aorta  consists  of  a  narrowing  of  the  vessel  at 
that  portion  which  extends  from  the  subclavian  artery  to  the 
ductus  arteriosus.  This  part  of  the  aorta  carries  before  birth 
only  part  of  its  full  quota  of  blood,  and  is  hence  small.  After 
birth,  when  the  side-track  path  of  the  ductus  arteriosus  is  occluded, 
it  assumes  its  full  function  and  enlarges.     Two  types  of  coarction 

'  (jowcr.s:   IJi.sf.'ascis  of  tho  Nervouw  System,  IS9'2,  p.  'MS. 
2  AUbutt:  System  of  Medicine,  1898,  vol.  vi,  p.  908. 


52  STUDIES  IN  CARDIAC  PATHOLOGY 

have  been  described :  (a)  Infantile,  consisting  of  a  diffuse  narrowing 
of  the  isthmus,  developmental  in  origin.  These  cases  die  early. 
(6)  Adult,  consisting  of  an  abrupt  cord-like  obstruction  near  the 
end  of  the  ductus  arteriosus.     (See  Fig.  83.) 

Pathologic  Physiology. — Owing  to  the  obstruction  to  ventric- 
ular outflow  blood-pressure  is  very  greatly  increased  in  the  left 
ventricle,  and  this  chamber  empties  itself  much  more  slowly 
and  gradually  than  normal.  Left  ventricular  systole  may  con- 
sume from  5  to  50  per  cent,  more  than  the  normal  time,  and  blood- 
pressure  in  this  chamber  may  even  rise  to  twice  the  normal.     Such 


Fig.  16. — Mitral  Stenosis. 

L.  F.,  male,  white,  aged  thirty-five  years.  (Philadelphia  Hosjjital.  vol.  xxiii,  p.  1. 
Physician:  Dr.  F.  P.  Henry.     Pathologist:  Dr.  Karsner.) 

Clinical  Notes:  At  one  time  chorea;  some  time  after,  while  lifting  a  heavy  weight,  he 
felt  something  give  way  in  the  chest,  and  has  been  unable  to  work  since.  He  is  an  intelligent 
mechanic,  who  has  been  under  observation  in  this  hospital  for  several  years.  Symptoms: 
Cyanosis,  dyspnea,  edema,  arrhythmia  (extrasystolic),  tachycardia,  pulsating  liver,  jugular 
veins,  etc.  Signs  of  double  mitral  and  tricuspid  lesion.  Died  gradually  with  symptoms  of 
pneumonia. 

Pathologic  Diagnosis:  Cloudy  swelling  of  heart,  with  double-sized  dilatation.  Mitral 
stenosis;  tricuspid  insufficiency.  Chronic  congestion  of  lungs;  hypostatic  pneumonia  of 
right;  beginning  gangrene  of  left.  Cyanotic  induration  of  kidneys;  arteriosclerosis;  chronic 
congestion  with  fatty  degeneration  of  liver,  also  slight  perilobular  fibrosis,  etc. 

Pericardium:  sniooth  and  glistening,  contains  150  c.c.  of  serous  fluid. 

Heart:  is  large,  soft  and  flabby;  weighs  580  gm.  Epicardium  shows  a  few  areas  of 
thickening  about  the  apex.  The  muscle  cuts  with  ease,  and  shows  a  light  brown,  slightly 
striated,  bleeding,  and  friable  surface.  Left  ventricular  wall  measures  11  mm.  Aortic  orifice, 
6.5  cm.,  and  shows  moderate  general  thickening  of  the  valve  leaflets,  and  slight  sclerosis  of 
the  sinus  of  Valsalva.  Mitral  orifice  ivas  not  incised;  its  leaflets  are  enormously  thickened  and 
contracted,  showing  at  the  right  junction  slight  calcification;  the  whole  ■presenting  the  appearance 
of  the  funnel-shaped  buttonhole  mitral.  The  chordae  tendinece  are  enormously  thickened,  retracted 
and  adherent,  and  are  attached  to  papillary  muscles  which  are  much  elongated  and  have  sclerotic 
tips.  The  fibrosis  of  the  anterior  mitral  leaflet  extends  forward  along  the  septum,  beloiv  the  bases 
of  the  aortic  valves,  producing  a  thickening  which  extends  transversely  through  the  bundle  of  His. 
The  ventricular  cavity  is  enlarged,  contains  chicken-fat  clot,  and  well  shows  flattening  of  the  col- 
umnae  earner.  Right  ventricular  wall,  4  mm.  Auriculo-ventricular  orifice  measures  15  cm.; 
shows  leaflets  which  are  moderately  thickened  along  the  free  edge.  Chordae  tendineae  thick- 
ened and  retracted.  Pulmonary  orifice  9  cm.;  shows  general  thickening  of  the  valves  and 
sclerosis  of  the  sinuses.  Pulmonary  artery  shows  slight  plaque-like  sclerosis.  Endocardium 
generally  normal.     Coronary  artery  moderately  sclerosed. 

(For  several  years  previous  to  this  patient's  death  the  author  had  from  time  to  time  oppor- 
tunities of  studying  the  heart  by  means  of  the  cardiosphygmograph.  Very  marked  arrhythmia 
was  always  present  and  consisted  of  the  type  which  Mackenzie  describes  as  "nodal  rhythm," 
the  "pulsus  irregularis  perpetuus"  of  Hering,  but  which,  according  to  more  recent  investiga- 
tions, is  probably  due  to  auricular  fibrillation.  This -is  of  especial  interest  in  view  of  the 
extensive  fibrons  in  the  region  of  the  auriculo-ventricular  bundle.) 


54  STUDIES  IN  CARDIAC  PATHOLOGY 

a  state  of  affairs  naturally  causes  a  stasis  and  an  increased  pres- 
sure in  the  left  auricle  and  in  the  pulmonary  circulation,  so  that 
hypertrophy  of  the  left  ventricle  and  auricle,  and  in  time  of  the 
right  heart,  occurs. 

Up  to  a  certain  point  the  tendency  of  the  left  ventricle  to 
hypertrophy  is  prevented  by  the  prolongation  of  the  presphygmic 
period,^  a  fact  which  gives  the  ventricle  a  longer  time  in  which 
to  empty  itself.  But  since  this  prolongation  of  the  presphygmic 
period  s  only  limited,  sooner  or  later  hypertrophy  must  occur, 
owing  to  the  increased  demand  for  work.  When  dilatation  of 
the  left  ventricle  appears,  a  relative  mitral  insufficiency  is  estab- 
lished, which  in  turn  and  in  time  leads  to  pulmonary  congestion, 
and  to  dilatation  of  the  right  heart. 

Clinical  Considerations. — The  frequency'  with  which  this  lesion 
is  tabulated  in  some  statistics  is  due  to  the  fact  that  they  were 
taken  from  clinical  and  not  from  autopsy  records.  A  systolic 
murmur  over  the  aortic  area,  especially  in  advanced  years,  is 
very  common,  and  results,  as  a  rule,  from  calcification,  stiffening, 
slight  roughening  of  the  orifice,  or  dilatation  of  the  aorta.  Such 
conditions  should,  of  course,  not  be  considered  an  "obstruction." 
(See  Fig  5.)  At  the  Philadelphia  General  Hospital  among  8,640 
autopsies  there  were  42  cases  of  aortic  obstruction  (0.47  per  cent.). 
Among  100  autopsies  in  Boston,  Jackson-  found  5  cases,  one  well 
marked.  Aortic  obstruction  occurred  in  5  per  cent,  of  1,781  cases 
of  heart  disease  at  the  Johns  Hopkins  Hospital, ■■*  and  in  2.73  per 
cent,  of  Romberg's  cases. 

When  any  considerable  degree  of  obstruction  exists,  it  is  usual!}' 
associated  with  insufficiency.  Aortic  disease  occurs  with  especial 
frequency  in  the  American  negroes,  a  fact  which  is  doubtless  due 
to  the  prevalence  of  syphilis  among  them. 

^  Gad  and  Luederitz:  Zeitschrift  f.  klin.  Medizin,  xx,  p.  374. 

-  Jackson:  Boston  Med.  and  Surg.  Jour.,  1896,  p.  12-1. 

'  Hirschfelder:  Diseases  of  the  Heart  and  Aorta,  1910,  p.  382. 


DISEASES    OF   THE    AORTIC    ORIFICE  55 

AORTIC  INSUFFICIENCY 

Pathologic  Anatomy  and  Occurrence. — Incompetence  of  the 
aortic  valves  generally  results  from  disease  of  the  leaflets,  although 
leakage  from  dilatation  of  the  aorta  is  occasionally  accountable 
for  the  condition.  Fibrosis,  which  generally  acts  by  thickening, 
stiffening,  retraction,  or  uneven  contraction  of  the  cusps,  is  gener- 
ally responsible  for  the  lesion.  Such  changes  are  often  associated 
with  disease  of  the  root  of  the  aorta,  and  hence  the  coronary 
arteries.  With  advancing  years  the  aortic  leaflets  increasingly  show 
the  signs  of  wear  and  tear  by  a  thickening,  and  curling,  so  that 
the  margins  fail  to  overlap.  Endocarditic  vegetations,  ulcerations, 
and  perforations  of  variable  shape,  size,  and  consistency  are  also 
responsible  for  a  certain  number  of  instances,  but  when  such  is 
the  case  the  incompetency  is  apt  to  be  associated  with  obstruction. 
Pure  isolated  aortic  insufficiency  is  generally  sj^philitic  or  arterio- 
sclerotic in  origin.  It  is  rare  in  children,  and  relatively  freciuent 
in  men  of  laborious  occupations,  especially  after  forty  years  of 
age,  and  among  syphilitics.  It  more  commonly  follows  pneumo- 
coccus  and  gonococcus  endocarditis  than  that  which  occurs  in 
rheumatic  fever  and  chorea.  Occasionally  aortic  insufficiency  is 
produced  very  early  in  certain  cases  of  severe  infective  endocarditis 
in  which  there  has  been  a  rapid  ulcerative  destruction  of  the 
leaflets,  but  generally  its  production  occurs  slowly  and  insidiously. 
Among  the  rarer  causes  of  aortic  insufficiency  valvular  rupture 
resulting  from  strain  or  trauma,  and  congenital  malformation  of 
the  cusps,  may  be  mentioned. 

In  addition  to  the  foregoing  changes  the  following  are  generally 
seen:  Thickening  or  atrophy  of  the  endocardium;  thickening 
of  the  free  margins  of  the  valves;  atrophy  of  the  trabecular 
muscles  with  connective-tissue  infiltration;  hypertrophy  and  dila- 
tation of  the  ventricular  muscle;  also  minute  warty  vegetations, 
the  result  of  recent  infection.  The  thickening  of  the  free  valvular 
margins  is  constant  in  aortic  insufficiency,  at  times  cylindrical,  at 


56  STUDIES  IN  CAHDIAC  PATHOLOGY 

others  irregular  in  shape.  One,  two,  or  all  of  the  leaflets  may 
be  involved.  The  right  cusp  suffers  most  frequently  and  exten- 
sively. The  valve  flaps  may  be  normal  in  size  or  even  larger. 
Trabecular  atrophy  is  most  marked  in  the  left  wall  of  the  ventricle 
near  the  apex.  Wasting  and  flattening  of  the  medial  papillary 
muscle  is  common,  as  is  also  localized  fibrosis  of  the  subendo- 
cardial muscle,  chiefly  in  the  outer  wall. 

Zahn^  has  described  as  anatomically  diagnostic  of  aortic  in- 
sufficiency, (a)  localized  thickening  of  the  interventricular  septum, 
and  (b)  parallel,  bow-shaped  lines  of  varying  thickness,  composed 
of  connective  tissue,  running  at  right  angles  to  the  cardiac  axis 
and  parallel  to  the  aortic  leaflets,  on  the  endocardium  of  the  ven- 
tricular septum.  He  attributes  their  formation  to  the  constant 
downward  pressure  of  the  regurgitating  blood,  although  he  admits 
that  the  elasticity  and  contraction  of  the  heart  muscle  might  play 
an  etiologically  contributing  role. 

Lately  Schminke^  has  reported  an  exaggeration  of  this  process 
in  which  the  redundant  endocardial  folds  both  on  the  septum  and 
on  the  ventricular  wall  form  small  pockets — actual  sacculations 
which  are  reproductions  in  miniature  of  the  valves  themselves. 
He  believes  that  these  pockets  indicate  a  functionally  compensating 
action  on  the  part  of  the  endocardium,  through  the  agency  of 
which  the  regurgitation  of  blood  is  diminished.  He  attributes 
their  genesis  to  a  process  similar  to  that  by  means  of  which  the 
semilunar  valves  develop  in  the  fetal  heart. 

(Before  the  truncus  arteriosus  divides,  four  folds  of  gelatinous 
tissue  covered  by  endocardium  are  formed,  two  of  which,  on  di- 
vision of  the  truncus  arteriosus  into  the  aorta  and  the  pulmonary 
artery,  are  cut  in  half,  so  that  each  vessel  gets  three  folds  which 
subsequently  take  on  the  form  of  pockets,  a  metamorphosis  in 
which  the  mechanical  action  of  the  blood-stream  jDrobably  plays 
a  role.) 

1  Zahn:   Verhandlung.  d.  Kongr.  f.  inn.  Med.,  189.5,  p.  351. 
-  Schminke:  Virchow's  Archives,  1908,  cxcii,  p.  50. 


Fig.  17. — Sclerotic  Endocarditis. 

L.  B.,  male,  Italian,  aged  seventy-seven  years.  (Philadelphia  Hospital  vol.  xxiv,  p.  97. 
Physician:   Dr.  A.  A.  Eshner.     Pathologist:   Dr.  H.  T.  Karsner.) 

Clinical  Notes:  Patient  was  admitted  in  a  delirious  condition.  The  heart  is  enlarged 
and  its  sounds  are  weak.  No  distinct  murmurs  are  heard.  The  urine  is  albuminous.  Hem- 
oglobin, 68  per  cent.;  erythrocytes,  5,200,000.  Death  occurred  gradually,  preceded  bj'  an 
extensive  and  a  generalized  purpuric  cutaneous  erruption. 

Pathologic  Diagnosis:  Emphysema,  hypostatic  pneumonia,  chronic  interstitial  myo- 
carditis, sclerotic  endocarditis  of  all  the  valves,  chronic  interstitial  nephritis,  etc. 

Heart:  Weighs  360  gm.  The  left  ventricle  mea.9ures  13  mm.  The  mitral  orifice  11  cm. 
Its  leaflets  and  chordae  tendineae  show  slight  general  thickening  and  rd  r:icl  ion.  The  i)aiiillary 
muscles  are  fibrosed.  The  aortic  orifice  measures  7.5  cm.  Its  IcoJIcIk  mr  llilrl.iiir,!  <tiiil  nl  Iheir 
bases  slightly  calcified.  The  sinus  of  Valsalva  is  sclerotic,  this  changr  innilvimj  llif  coromirij  ori- 
fices. The  right  ventricular  wall  measures  6  mm.,  and  the  tricuspid  orifice  9  cm.,  its  leaflets 
being  thickened.  The  pulmonic  orifice  measures  8.5  cm.;  its  leaflets  are  thickened,  as  is  also 
the  ventricular  endocardium.     The  coronary  arteries  are  sHghtly  sclerotic. 

This  .specimen  illustrates  the  type  of  case  in  which  the  disease  of  the  aortic  leaflets  is  the 
primary  and  the  main  lesion,  the  aorta  itself  being  relatively  uninvolved.  (Compare  with 
F'igs,  52  and  53.) 


58  STUDIES  IN  CARDIAC  PATHOLOGY 

Experimental  section  of  the  aortic  valves  is  followed  almost  at 
once  by  a  fall  of  the  diastolic  pressure,  by  dilatation  of  the  left 
ventricle,  and  sooner  or  later  by  the  establishment  of  a  mitral 
insufficienc3^  In  man  the  occurrence  of  the  latter  has  been 
regarded  as  beneficial,  on  the  assumption  that  the  leak  acts  as 
a  safety-valve,  just  as  does  tricuspid  dilatation  in  the  right  heart 
during  muscular  strain.^ 

Some  unusual  and  curious  aortic  cases  have  been  recorded. 
Thus,  Tegeler'  reported  a  case  in  which  a  revolver  bullet  was 

1  Taylor:  Brit.  Med.  Jour.,  June  23,  1906. 

^Tegeler:  Mtlnch.  med.  Woch.,  1909,  No.  34,  p.  1740. 

Fig.  18. — Chronic  Mural  and  Aortic  Endocarditis. 

O.  G.,  male,  white.  (Pennsylvania  [Hospital.  Autopsy:  1133.  Physician:  Dr.  New- 
lin.     Pathologist:  Dr.  Krumbhaar.) 

Clinical  Notes:  Denies  syphilis.  Gonorrhea  fifteen  years  ago,  followed  three  months 
later  by  severe  arthritis.  Complains:  Abdominal  pain,  constipation,  headache,  cough  with 
slight  expectoration,  pain  after  food,  eructations,  orthopnea,  edema. 

Heart:  Second  space  3.5  cm.  to  right  of  mid-sternal  line;  fifth  space  12. .5  cm.  to  left  of 
mid-sternal  line.  Action  is  regular.  Sounds  weak  and  soft.  Distinct  double  apical  murmur 
transmitted  to  axilla  and  base,  loud  at  the  aortic  area.  Water-hammer  pulse.  Blood-pressure : 
135  mm.;  diastohc  82  mm.  (Stanton).  Urine:  Albumin  and  casts.  Death:  Gradual  with 
delirium  and  coma. 

Pathologic  Diagnosis:  Chronic  mural  and  aortic  endocarditis  with  incompetency.  Gen- 
eral arteriosclerosis,  cardiac  hypertrophy  and  dilatation.     Chronic  diffuse  nephritis,  etc. 

Pericardium:   Contains  50  c.c.  slightly  turbid  fluid  containing  flakes. 

Heart:  Enormously  dilated  (15  x  14  x  9  cm.).  Weighs  600  gm.  Large  milk  spot  on 
anterior  surface  of  right  ventricle,  and  a  few  small  ones  posteriorly.  Over  the  auricular  sur- 
face numerous  minute  reddish  points.  Muscle  of  the  left  ventricle  hght  red  streaked  with 
yellow,  but  the  right  ventricle  is  pale  and  yellow.  Currant-jelly  clot  in  right  side  of  heart  and 
in  auricular  appendage.  Right  auriculo-ventricular  valves  normal.  Muscle  6  to  8  mm. 
Left  auricle  and  ventricle  also  currant-jelly  clots.  Mitral  valve  is  not  much  thickened,  but  is 
shrunken  and  apparently  incompetent.  Aortic  valves  are  diffusely  thickened,  and  the  aorta  shows 
general  sclerosis.  The  endocardium,  especially  of  the  septum,  shows  peculiar  raised  white  streaks 
of  an  irregular  padding  which  measure  2  mm.  in  diameter  and  project  from  the  surface  2  mm. 
Just  below  the  aortic  valves  there  is  a  diffuse  thickening  of  the  endocardium,  which  extends  into  the 
aortic  valve  for  some  distance,  and  also  into  the  mitral  leaflets.  Left  ventricular  muscle  14  to  IS  mm.; 
normal  in  color  and  firm.  Its  cavity  shows  some  dilatation.  The  coronary  arteries  are  scler- 
otic near  their  origin,  but  the  small  branches  are  thin  and  delicate.  Valves:  Tricuspid  12; 
pulmonary  8;   aortic  9;   mitral  11  cm.  in  circumference. 

Microscopic  Examination:  Immediately  beneath  the  endocardium  the  muscle-fibers  are 
much  swollen,  granulated  and  vacuolated,  with  ragged  edges.  They  have  lost  their  striae. 
Nuclei  are  large,  and  in  the  longitudinally  cut  fibers  vacuoUzation  is  found  to  be  most  marked 
about  the  nuclei.  This  process  is  well  marked  in  the  papillary  muscles,  their  endocardial 
covering  being  thickened.  There  is  a  slight  diffuse  increase  of  delicate  fibrous  tissue.  In 
some  places  this  is  sufficiently  marked  to  produce  atrophy  and  degeneration  of  the  muscle- 
fibers. 


60  STUDIES  IN  CARDIAC  PATHOLOGY 

unexpectedly  found  encysted  in  an  aortic  cusp,  in  a  man  who  was 
accidentally  killed  by  other  causes.  In  Jacobi's  case,^  which 
appeared  to  be  traumatic  in  origin,  the  heart  murmurs  could  be 
heard  across  the  room.  The  question  of  foreign  bodies  in  the 
heart  has  been  studied  b.y  Zesas,-  who  collected  118  cases. 

Pathologic  Physiology. — Owing  to  the  increased  amount  of 
blood  which  the  left  ventricle  is  called  upon  to  handle,  hyper- 
trophy and  dilatation  occur.  In  favorable  cases  when  the  nutrient 
supply  of  the  ventricle  is  sufficient,  this  process  goes  on  for  a 
long  time.  In  such  events  the  enormous  cor  bovis  is  produced,  an 
enlargement  greater  than  is  seen  in  any  other  form  of  valvular 
disease.  When  the  hj^pertrophic  growth  exceeds  the  nutritive 
supply,  however,  as  is  sooner  or  later  bound  to  occur,  degenerative 
changes  followed  by  dilatation  and  signs  of  insufficiency  occur. 
Or  it  may  be  that  before  these  changes  are  brought  about,  the  mitral 
valve,  owing  to  constant  overstrain,  by  virtue  of  either  actual 
damage  to  its  leaflets  or  dilatation  of  its  sphincter,  becomes 
markedly  insufficient,  and  thus  a  pulmonary  congestion  is  brought 
about.  The  marks  of  wear  and  tear  upon  the  left-sided  valves, 
and  upon  the  whole  arterial  system,  in  this  form  of  valvular 
disease  are  very  pronounced.  The  incessant  pounding  of  the 
hypertrophic  ventricle,  the  high  systolic  and  low  diastolic  pressure, 
produce  a  very  intermittent  blood-supply,  which  of  course  affects 
the  coronary  arteries  as  well  as  those  of  the  whole  arterial  system. 
If  one-third  or  one-fourth  of  the  systolic  output  regurgitates, 
marked  hypertrophy  and  dilatation  will  of  course  occur;  but  if 
the  aortic  lesion  is  slight,  so  that  only  a  few  cubic  centimeters  of 
blood  flow  backward,  although  a  diastohc  murmur  may  be  heard, 
yet  enlargement  of  the  heart  may  not  be  sufficient  to  be  clinically 
demonstrable  (Krehl). 

The  experiments  of  Henderson,  Stewart/  and  Moritz  indicate 
that  much  less  blood  regurgitates  in  aortic  insufficiency  than  has 

'  Jacobi:  New  York  Med.  Jour.,  Aug.  9,  1902. 

-  Zesas:  Fortschritte  in.  d.  Medizin,  1910,  xxviii,  p.  649. 

'  Henderson:  Archives  of  Internal  Medicine,  Jan.,  1908. 


I''ir;.  10, — Aortic  f>B.sTuucTiox,  Seen  from  Above. 

The  leaflfits  are  fused  together,  thickened,  and  indurated.     Tliey  are  covered  witli  small 

vegetations. 


62  STUDIES    IN    CARDIAC    PATHOLOGY 

hitherto  been  supposed.  This  is  owing  to  an  increased  tonicity 
which  the  left  ventricle  assumes.  The  marked  fluctuations  of 
blood-pressure  which  occur  in  these  cases  seem  to  be  due  to  a  reflex 
lowering  of  the  diastolic  pressure.  This  is  borne  out  by  the  well- 
known  clinical  fact  that  diastolic  pressure  often  ranges  between 
40  and  60  mm.  Hg,  even  where  compensation  is  fairly  well  main- 
tained, while  the  systolic  pressure  is  often  as  high  as  180  mm. 
The  amount  of  regurgitation  depends  upon  the  severity  of  the 
lesion  and  the  efficiency  of  compensation  in  the  myocardium, 
especially  of  the  left  ventricle  and  of  the  left  auricle. 

Until  quite  recently  it  was  generally  believed  that  aortic 
insufficiency  was  due  to  the  same  causes  as  those  which  produce 
an  obstruction  or  sclerotic  change.  Although  this  is  no  doubt 
true,  yet  recent  investigations  point  very  strongly  toward  the 
fact  that  a  large  number,  if  not  the  majority,  of  cases  of  isolated 
aortic  insufficiency  are  the  result  of  syphilis.  The  association 
of  this  lesion  with  locomotor  ataxia  has  long  been  noted,  ^  and 
recently  it  has  been  shown  that  a  very  large  proportion  of  cases 
of  aortic  insufficiency  give  a  positive  Wassermann  reaction,^ 
while  mitral  cases  do  so  only  exceptionally.  The  spirocheta 
pallida  has  been  demonstrated  in  these  lesions.^ 

The  possibilit}^  of  a  relative  or  functional  aortic  insufficiency 
has  been  much  discussed,  and  seems  to  have  been  definitely 
established  by  having  been  experimentally  produced  by  Thayer 
and  MacCallum.*  But  certainly  the  vast  majority  of  cases  of 
this  lesion  seen  in  practice  result  from  actual  valvular  damage — 
thickening,  shrinking,  perforation,  stiffening,  roughening,  or 
calcification  of  the  aortic  cusps.  It  can  be  easil)^  understood 
that  where  such  changes  as  those  just  mentioned  are  present, 

'  Babinski:  Soc.  Med.  des  Hopit.,  Paris,  1901,  Nov.  14  and  21.  Strlimpell:  Deut.  med. 
Woch.,  1907,  No.  47.     Schiitze:  Deut.  Zeit.  f.  Chir.,  1908,  1-5,  etc. 

-  Danielopolu:  Bull.  Soc.  Biolog.,  Paris,  May  30,  1908.  Collins  and  Sachs;  Amer. 
Jour.  Med.  Sci.,  Sept.  1909.  Debove  and  Tremolieres:  Jour.  Med.  Franijais,  April,  1910. 
Longcope:   Jour.  Am.  Med.  Assoc,  1909.     Pasaschivescu:  These  de  Bucarest,  1910. 

^Wright  and  Richardson:  Bo.ston  Med.  and  Surg.  Jour.,  April  29,  1909. 

*  Thayer  and  MacCallum:  Amer.  Jour.  Med.  Sci.,  Feb.,  1907. 


DISEASES    OF   THE    AORTIC    ORIFICE  63 

both  obstruction  and  insufficiency  are  apt  to  result,  and  such  is 
generally  the  case — a  pure  insufficiency  or  obstruction  being  the 
exception. 

Clinical  Considerations. — Aortic  insufficiency  may  exist  with- 
out an  audible  murmur,  and  even  when  such  is  present  it  is  apt 
to  be  low-pitched  and  difficult  to  hear.  Jackson  found  that  this 
was  the  most  frequently  overlooked  valvular  lesion  in  100  autopsies. 
Animal  experimentation  has  further  corroborated  the  foregoing 
statements.  In  advanced  life  relative  aortic  insufficiency  is 
favored  by  the  fact  that  both  the  diameter  and  the  length  of  the 
aorta  increase  with  time,  while  its  elasticity  diminishes.^ 

'Scheel:  Virchow's  Arcliiv,  cxci,  1908. 


IV.  DISEASES  OF  THE  MITRAL  ORIFICE 
MITRAL  OBSTRUCTION 

Varieties. — From  an  etiologic  standpoint  there  are  three  varieties 
of  this  lesion:  (a)  infectious;  (b)  arteriosclerotic;  (c)  congenital; 
the  first-named  being  probably  the  commonest.  Hensen  has 
reported  mitral  stenosis  as  the  result  of  pressure  from  a  thoracic 
aneurism.  Morgagni  reported  one  due  to  the  pressure  of  a  calcified 
pericardium.  A  functional  form  of  mitral  stenosis,  supposedly 
due  to  nervous  influences,  occurring  chiefly  in  neuropaths  and 
chlorotics,  as  the  result  of  orificial  constriction  or  retroversion  of 
the  leaflets  from  the  regurgitating  blood  of  an  aortic  insufficiency, 
has  been  described  especially  in  the  French  literature.^  Its 
existence  rests  upon  purely  hypothetic  grounds,  and  is  very 
questionable. 

From  the  anatomic  standpoint  four  varieties  are  recognized: 
(a)  buttonhole;  (6)  funnel-shaped;  (c)  vegetative;  (d)  cystic 
(due  to  valvular  aneurism). - 

The  mitral  orifice  in  men  averages  110.37  mm.,  in  women 
92.68  mm.  in  circumference.  The  mitral  and  tricuspid  valves 
show  the  greatest  difference  in  size  when  the  sexes  are  compared, 
a  fact  which  probably  has  some  bearing  on  the  preponderance  of 
stenosis  of  these  orifices  in  women. 

It  has  been  shown  that  the  large,  freely  movable  anterior 
mitral  leaflet  has  a  somewhat  different  function  from  the  small, 
relatively  fixed,  posterior  leaflet,  in  that  the  former,  in  addition 
to  preventing  regurgitation  into  the  auricle  during  ventricular 
systole,  actually  forms,  together  with  the  interventricular  septum, 
a  channel  which  helps  to  conduct  the  ventricular  contents  into 

'Bard;  Semaine  M6d.,  1906,  No.  20.  Lepine:  Provence  Medic,  xx,  No.  2.  Cecone: 
Riforma  Medic,  July  27,  1908. 

=  Cruveilhier:  Anat.  Path.,  ii,  1852. 


66  STUDIES  IN  CARDIAC  PATHOLOGY 

the  aorta  ^  (the  "Stromrinne"  [flume]  of  Oesterreich -).  It  has 
thus  a  double  function,  and  pathologic  alterations  in  its  structure 
have  a  double  result.  In  this  connection  Beitzler  ■'  considers  the 
white  spots  frequently  to  be  found  on  the  ventricular  surface 
of  the  anterior  mitral  leaflet  as  mechanical  and  not  inflammatory 
in  origin,  due  to  conditions  similar  to  those  which  are  active  in 
the  production  of  aortic  sclerosis.  Looked  at,  then,  from  the 
standpoint  of  physiology,  this  surface  of  the  anterior  leaflet  is 
really  a  part  of  the  aorta.  The  fact  that  this  leaflet  is  so  much 
oftener  diseased  than  the  others  has  also  been  explained  as  due 
to  greater  tension  when  closed  (Sibson),  a  smaller  line  of  contact 
during  closure,  greater  tendinous  traction,  greater  vascularit.y, — 
favoring  embolic  processes.  It  should  also  be  borne  in  mind  that 
the  anatomic  relationship  of  the  mitral,  tricuspid,  and  aortic 
valves  is  a  very  intimate  one.     (See  Figs.  7  and  8.) 

Pathologic  Anatomy. — IMitral  stenosis*  may  or  may  not  begin 
as  an  insufficiencj',  which,  through  gradual  adhesion  of  the  leaflets 
and  contraction  of  the  surrounding  tissues,  ends  as  a  combined 
lesion,  sometimes  passing  through  a  stage  of  firm  obstruction. 
When  the  free  edges  of  the  leaflets  are  chiefly  involved,  the  well- 
known  funnel-shaped  oriflce,  which  is  generally  seen  in  early  life, 
results.  (See  Figs.  16  and  22.)  When  mechanical  pressure  factors 
have  existed,  as  in  the  cases  occurring  in  chronic  nephritis,  the 
leaflets  are  less  affected,  and  the  lesion  consists  more  of  a 
thickening,  hardening,  shortening,  and  sometimes  a  calcification  of 
the  papillary  muscles  and  chordae  tendinese.  "The  insertions  of  the 
chordae  tendinese  are  spread  out  over  the  greater  part  of  the  lower 
surface  of  the  leaflets,  and  when  there  is  long-continued,  high,  intra- 
cardiac pressure,  the  whole  valve  becomes  very  much  thickened, 
and  there  is  a  great  increase  in  the  fibrous  tissue,  which  eventu- 
ally leads  to  the  puckering  or  contraction  of  the  segments,  and  the 

■  Arch.  f.  exp.  Path.  u.  Pharm.,  1907,  Ivii,  .57. 

-  Virchow's  Arch.,  Ixi,  pp.   180,  196. 

'  Virchow's  Arch.,  1901,  Ixi,  343. 

*  Heitz  and  Sezary:  Arch,  de  Mai.  du  Coeur,  Dec.  1,  1908. 


DISEASES    OF   THE    MITRAL    ORIFICE  67 

diaphragmatic  or  buttonhole  variety  is  produced."^  (See  Fig.  24.) 
Some  writers — Haj^den,  Sanson,-  Hilton,  and  Fagge — have  held 
that  the  funnel  shape  is  almost  exclusively  that  of  youth,  and  the 
buttonhole  form  that  of  adult  life.  Barr  suggests  that  it  is  largely 
a  question  of  the  duration  of  the  lesion,  and  that  long-standing 
cases,  with  marked  infiltration,  sclerosis,  and  contraction  (and 
these  are  the  conditions  which  obtain  later  in  life),  develop  the 
buttonhole  shape. 

"  In  some  cases  the  mitral  cusps  are  so  thickened  and  contracted 
that  they  mereh'  form  a  transverse  septum  with  a  narrow  slit 
between  auricle  and  ventricle.  In  such  cases  the  chordae  tendinese 
are  frequently  thickened  and  matted  together,  and  the  papillary 
muscles  in  such  a  fibroid  condition  that  it  would  seem  impossible 
for  a  first  sound  to  be  generated  by  the  mitral  valve." 

A  congenital  form  is  frequently  discussed,  especially  in  the 
French  literature.  It  is  described  as  often  of  the  funnel-shaped 
type,  produced  by  fusion  of  the  leafiets,  which  are  said  to  resemble 
other  congenital  lesions  n  that  they  present  no  signs  of  inflamma- 
tory changes — thickening,  contraction,  etc.  It  is  sometimes  asso- 
ciated with  other  developmental  anomalies,  such  as  hare-lip. 
Occasionally  it  occurs  together  with  infantilism,  myxedema,  etc.^ 
Other  observers  consider  that  these  lesions  result  from  a  fetal 
endocarditis.  The  symptoms  in  these  cases  appear  between  the 
seventh  and  fourteenth  years,  the  period  in  which,  despite  rapid 
bodily  growth,  the  heart  remains  almost  at  a  standstill. 

According  to  Bizot  and  Beneke,  the  heart,  which  is  perfectly  formed  by  the 
seventh  week  after  conception,  doubles  its  size  between  the  time  of  birth  and  the 
age  of  twenty-four  months,  and  again  between  three  and  seven  years.  It  re- 
mains almost  stationary  from  seven  to  fifteen  years,  and  again  increases  one- 
third  of  its  size  between  fifteen  and  twenty  years,  at  which  time  normal  growth 
practically  ends.'' 

'  .J.  Barr:  Lancot,  Doc.  19,  1908,  p.  17S9. 

'San.son  CAllbutt's System;:  In  children  one  "buttonhole"  is  seen  to  eight  funnels,  where- 
a.s  in  adults  there  is  one  funnel  to  twenty-five  "buttonholes." 
'  K'ippel  and  Chabrol:  Rev.  de  M6d.,  1910,  p.  1.53. 
'Quoted  Pawlinow:   "Kongcnitale  Mitral  Stenose,"  Berlin,  1909,  p.  (5. 


68  STUDIES  IN  CARDIAC  PATHOLOGY 

Quenus  '■  states  that  the  mitral  valves  are  developed  in  the  second  and  third 
months  of  fetal  life,  existing  at  first  as  muscle-fibers  which  at  the  beginning  of  the 
fourth  month  are  transformed  into  connective  tissue.  It  is  in  this  stage  of 
embryonic  life  that  congenital  lesions  would  be  produced. 

Pawlinow  states  that  in  congenital  mitral  stenosis  neither  the  right  ventricle 
nor  left  auricle  hypertrophy,  owing  presumably  to  nutritional  defect.  The 
leaflets  themselves  are  thinner,  weaker,  more  delicate,  and  are  more  easily  torn 
than  normal  ones.  He  believes  that  the  cases  of  mitral  stenosis  which  Pitt  ~ 
describes  as  so  frequently  associated  with  chronic  nephritis  are  cases  of  congenital 
mitral  stenosis,  and  that  this  congenital  form  predisposes  to  infections.  The 
heart  is  smaller,  but  the  patient's  life  longer,  than  in  the  acquired  lesions,  for 
despite  the  fact  that  many  cases  develop  pulmonary  tuberculosis,  the  latter 
tends  to  run  a  prolonged  course.  This  association  of  mitral  stenosis  and  pul- 
monary tuberculosis  was  explained  by  Potain  as  due  to  toxemia. 

The  belief  that  mitral  stenosis  is  often  a  result  of  acquired 
or  hereditar}^  pulmonary  tuberculosis,  was  first  enunciated  by 
Tripier,''  and  notabi}'  elaborated  by  Potain  *  and  Teissier.  °  A  full 
discussion  of  this  hypothesis  would  lead  too  far.  Suffice  it  to  say 
that  this  view  that  mitral  stenosis  may  be  caused  by  the  toxin 
of  the  tubercle  bacillus  is  not  generally  accepted.  Hereditary 
syphilis  has  also  been  described  as  a  cause.'' 

The  normal  auricular  capacity  ranges  between  40  and  70  cm. 
(average  55  cm.).  In  mitral  stenosis  these  figures  may  be 
greatly  increased.  In  one  case  reported  by  Briquet '  the  enormous 
proportions  of  650  cm.  were  reached — practicallj'  equal  to  the 
size  of  a  whole  normal  heart.  Auricular  hypertrophy  is  insignifi- 
cant compared  to  what  ma.y  occur  in  the  ventricle,  nevertheless 
an  increase  to  the  thickness  of  3  cm.  has  been  observed.^     Atrophy 

'  Quenus:  These  de  Paris,  18S3,  p.  42. 

-  Pitt,  at  Guy's  Hospital,  found  that  mitral  stenosis  occurred  three  times  as  often  in 
association  with  renal  sclerosis  as  in  other  diseases,  and  that  two-thirds  of  the  cases  occur  in 
women. 

'Tripier:  Arch,  de  MM.  Exper.,  ISSS. 

*  Potain:  Jour,  de  Med.  et  de  Chir.  Prat.,  1891. 

5  Teissier:  These  de  Paris,  1894.  Sears  (St.  Paul  Med.  Jour.,  March,  1907)  found  well- 
marked  tuberculosis  in  11  or  22  per  cent,  of  the  Boston  City  Hospital  cases.  A  number 
of  other  cases  showed  chronic  pleuritis,  which,  if  counted  as  tuberculous  lesions,  would  raise 
the  percentage  to  40.  Crawford  in  112  autopsies  found  pleuritis  48  times,  but  definite  tuber- 
culosis only  twice. 

*  Labadie,  Lagrave,  and  Deguy:  Jour,  des  Prat.,  July,  1899. 
'  Briquet:  These  de  Paris,  1890,  case  xix. 

«  Bourdcl:  Soc.  Anat.  Paris,  1880.     Samways:  These  de  Paris,  1896. 


Fifi.   21. — Chroxic   Aortk-   and   Mitral  ENDorARiuTis,   with  Hypertrophy   and   Dila- 
tation OF  THE  Left  Ventricle. 

The  aortic  valves  are  thickened  and  retracted.  The  aorta  above  them  shows  well-marked 
sclerotic  changes  involving  the  mouth  of  the  right  coronary  artery.  The  mitral  valve  is 
thickened,  retracted,  and  sclerotic.  The  predominant  lesion  in  each  instance  is  insufficiency. 
(Specimen  from  the  German  Hospital,  Philadelphia.) 


70  STUDIES   IN    CARDIAC    PATHOLOGY 

of  the  auricular  muscle  is  by  no  means  rare,  and  may  be  of  such 
extreme  degree  that  the  muscular  tissue  may  completely  disappear, 
leaving  only  a  fibrous  sac.^  When  the  auricle  is  thus  greatly 
distended,  its  functional  capacity  ceases,  as  is  shown  b)^  the  dis- 
appearance of  the  auricular  wave  in  the  jugular  (Mackenzie), 
in  the  esophogram  (Joachim),  and  in  the  volume  curve  (Hirsch- 
f elder).  .  Occasionally  enormous  dilatation  is  met  with,  as  in 
Mliller's  case,  in  which  the  left  auricle  was  larger  than  a  child's 
head,  and  the  heart  weighed  620  gm.,  the  patient's  bodily  weight 
being  onlj^  65  Kg.  (normal  relations:  heart,  297  gm.  to  body  of 
60  or  70  Kg.). 

According  to  Witwicki,-  the  left  auricle  is  the  most  distensible 
of  all  the  heart  chambers,  and  Samuelson''  has  stated  that  occlu- 
sion of  the  left  coronary  artery  produces  a  flaccid  dilatation  of  the 
left  auricular  wall.  Although  these  facts  may  be  correct,  the  left 
auricle  is,  owing  to  its  anatomic  relations,  much  less  likely  than 
the  right  to  expand,  since  such  an  occurrence  can  take  place  in 
but  one  direction,  viz.,  upward.  Owen  and  Fenton  have  reported 
a  left  auricle  with  a  capacity  of  900  c.c.,*  and  Minkowski'  has 
recorded  a  dilated  heart  which  contained  4  liters  of  blood, 
nearly  three  of  which  were  found  in  the  left  auricle.  In  such 
cases  the  auricular  wall  exists  as  a  mere  membranous  sack,  no 
thicker  than  a  visiting  card  (Sansom),  and  resembles  a  greatly 
distended  bladder.  Such  distention  by  dilation  of,  and  upward 
pressure  on,  the  left  pulmonary  artery  may  cause  left  recurrent 
laryngeal  paralysis  by  compression  of  this  nerve  between  the  last 
named  vessel  and  the  aortic  arch.  Ten  such  cases  with  autopsy 
reports  and  a  considerably  larger  number  of  clinical  observations 
are  now  on  record.     In  some  of  these  cases  direct  pressure  of  the 

'  Mtiller:  Zeit.  f.  klin.  Med.,  190.5,  hi,  p.  520. 

-'  Witwicki:  Zeit.  f.  kl.  Med.,  xxvii,  1895,  p.  321. 

'  Samuelson:  Ibid.,  vol.  ii. 

■•  Fetterolf  and  Norris:  "The  Anatomic  Explanation  of  Paralysis  of  the  Recurrent  Laryn- 
geal Nerve  Found  in  Certain  Cases  of  Mitral  Stenosis."  Trans.  Coll.  Phj-sicians  of  Phila- 
delphia, 1911,  Am.  Jour.  Med.  So.,  1911. 

5  Owen  and  Fenton:  Trans.  Clin.  Soc.  London,  M;iy  24,  1901. 


DISEASES    OF   THE    MITRAL    ORIFICE  71 

left  auricle  upon  the  aorta  has  been  described,  but  as  has  been 
shown  by  Fetterolf  and  myself  such  a  state  of  affairs  is  an- 
atomically impossible.^  Right  recurrent  paralysis  has  also  been 
described,  it  being  assumed  in  explanation,  and  without  post- 
mortem substantiation,  that  the  brachiocephalic  and  the  sub- 
clavian arteries  had  undergone  displacement. 

It  was  formerly  taught  that  mitral  stenosis  is  practically  always  associated 
with  insufficiency.  This  has  been  vigorously  contradicted,  and  much  discussion 
has  been  aroused.  Romberg  found  only  two  cases  of  pure  stenosis  among  670 
heart  cases.  Krehl  considers  it  very  rare,  and  some  chnicians  deny  its  existence 
altogether.  Hampeln,^  on  the  other  hand,  finds  pure  obstruction  in  from  10  to 
20  per  cent,  of  all  his  mitral  cases,  and  Schabert^  states  that  at  least  half  of  all 
the  mitral  lesions  at  the  Stadtkrankenhaus  at  Riga  are  pure  stenosis.  There 
can  be  no  question  that  in  a  good  many  cases  the  stenotic  is  the  serious  and 
evident,  and  the  insufficiency  the  slight  and  inconsequential  lesion.  Personally, 
although  I  have  seen  quite  a  number  of  cases  of  isolated  obstruction,  yet  it  is  my 
belief  that  the  lesion  is  much  more  commonly  a  mixed  one. 

Etiology. — The  great  majority  of  cases  of  mitral  stenosis, 
especially  those  of  early  life,  owe  their  existence  to  an  antecedent 
rheumatic  infection.  Following  this  in  frequency  come  chorea, 
arteriosclerosis,  and  infectious  processes  of  different  kinds,  including 
syphilis.  Chronic  interstitial  nephritis  is  also  not  infrequently 
associated  with  mitral  stenosis. 

Goodhart  in  192  cases  of  this  form  of  renal  disease  found  the  last-named 
valvular  lesion  in  about  25  per  cent.,  and  Pitt  states  that  mitral  stenosis  is  three 
times  as  common  in  patients  with  Bright's  disease  as  in  those  not  so  afflicted. 
Although  these  facts  are  doubtless  correct,  it  must  not  be  forgotten  that  in  these 
cases  the  valvular  disease  is  simply  a  part  of  a  general  arteriosclerosis,  in  which 
such  extreme  degrees  of  mitral  disease  as  are  seen  as  the  result  of  inflammatory 
lesions  are  distinctly  the  exception.  They  occur  in  individuals  more  advanced 
in  life,  present  quite  a  different  clinical  picture,  and  play  much  less  important  a 
role  in  the  production  of  death. 

Occurrence. — Among  4,791  autopsies  at  Guy's  Hospital, 
Samways  ^  found  196  cases  of  mitral  disease  in  which  the  orifice 

'  Minkowski:  Munch,  med.  Woch.,  Ivi,  igo."),  p.  1S2. 
^  Hampcln:  Dcut.  med.  Woch.,  1908,  p.  1.301. 
'Schubert:  Deut.  Arch.  f.  klin.  Med.,  1909,  p.  117. 

*  Sarnways:  Hrit.  Med.  Jour.,  1S98,  p.  364.  (AmonK  8,040  autopsies  at  (he  I'hil;i,ili'l|)hia 
Hospital  there  were  1  Id  well-marked  enses  of  milral  stenosLs.) 


72  STUDIES    IN    CARDIAC    PATHOLOGY 

measured  less  than  3J^  inches  (admitted  two  fingers  or  less). 
Minor  grades  of  stenosis  were  therefore  excluded.  In  108  cases 
the  orifice  measured  234  inches  (admitted  one  finger)  or  over, 
and  in  85  cases  measured  less  than  23^  inches,  three  cases  being 
doubtful;  107  cases  were  in  females,  89  in  males.  The  average 
age  at  the  time  of  death  among  the  former  was  33.6  years;  among 
the  latter,  43.6  years.  In  32  cases  tricuspid  obstruction  was 
also  present;  generally  this  occurred  in  the  severe  cases.  In  a 
large  proportion  of  cases  the  aortic  valve  was  also  thickened, 
•but  actual  stenosis  was  seldom  encountered.  Left  auricular 
hypertrophy  occurred  in  44  of  77  severe  cases,  and  in  21  of  96 
moderate  cases  (in  the  first  class  in  more  than  half,  in  the  second 
in  less  than  one-quarter).  Left  auricular  dilatation  was  marked 
in  14  of  77  severe,  slight  in  6,  the  data  being  incomplete  in  18 
cases.  Right  ventricular  hypertrophy  appeared  in  41  of  77  severe, 
and  25  of  96  moderate  cases.  Right  ventricular  dilatation  was 
present  in  40  out  of  77  severe,  and  27  of  96  moderate  cases.  The 
left  ventricle  was  generally  normal  or  small,  rarely  enlarged. 
Among  23  cases  dying  "surgical  deaths,"  only  4  had  dilated  left 
auricles.  Pericarditis  was  present  in  nearly  one-third  of  the  cases, 
and  sudden  death  occurred  in  7.  Sixty  per  cent,  of  the  cases 
gave  a  history  of  rheumatic  infection.  Nineteen  cases  were  ad- 
vanced in  life  and  gave  no  such  history,  showing  that  this  lesion 
TCiSLy  have  a  sclerotic  as  well  as  an  infectious  origin.  Nearly  all 
statistics  show  that  mitral  obstruction,  especially  the  form  which 
occurs  in  early  life  and  results  from  an  infectious  valvulitis,  is 
very  much  more  common  in  the  female  sex.  Various  explanations 
have  been  offered,  such  as,  for  instance,  that  prolonged  subacute 
infections  are  more  frequent  in  women,  also  that,  owing  to 
lessened  cardiac  activity  and  intracardiac  pressure,  the  mitral 
valve  makes  less  extensive  excursions,  and  is  hence  more  prone 
to  adhesive  changes.  Congenital  structural  differences  have  also 
been  suggested.  It  must  be  admitted,  however,  that  none  of 
these    explanations    are    satisfactory.     Among    50    autopsies    of 


Fig.  22. — Mitral  Stenosis. 
8|jccimen  .showing  mitral  stenosis  viewed  from  the  ventricular  side.     The  valvular  end<i- 
cardium  is  thickened  and  has  lost  much  of  its  flexibility;   the  chorda;  tendinea;  are  thickened, 
indurated,  contracted,  and  more  or  less  fused  together.     Small  verrucose  vegetations  are  seen 
on  the  ventricular  endocardium  just  to  the  left  of  the  mitral  valve. 


74  STUDIES    IN    CARDIAC    PATHOLOGY 

mitral  stenosis  cases  Sears  found  in  25  a  mitral  lesion  only  (19 
admitted  only  one  finger).  In  7  other  cases  the  mitral  lesion  was 
the  principal  one  (2  fibrous  pericarditis,  5  aortic  disease).  So 
that  in  27  cases  there  was  mitral  disease  alone,  in  17  mitral  and 
aortic,  in  1  mitral  and  tricuspid,  in  5  mitral,  aortic,  and  tricuspid, 
in  4  fibrous  pericarditis. 

Pathologic  Physiology. — The  presence  of  mitral  stenosis  at 
first  tends  to  produce  left  auricular  hypertrophy,  owing  to  obstruc- 
tion to  outflow  offered  by  the  constricted  orifice.  Hirschfelder  ^ 
and  Wolfsohn  have  shown  that  the  first  effect  of  mitral  stenosis 
as  indicated  by  the  volume  curve  is  to  slow  the  inflow  into  the 
ventricles.  "As  the  result  of  this  the  left  auricle  is  more  than 
usually  full  at  the  time  of  its  systole,  and  forces  an  unusually 
large  quantity  of  blood  into  the  ventricle."  The  capability  of 
the  auricle  to  hypertrophy  is  limited,  however,  and  great  thickening 
of  its  walls  is  rarely  seen.  With  continued  overwork  the  chamber 
elongates,  becomes  cone-shaped,  and,  as  nutrition  fails,  dilates. 
That  this  dilatation  is  not  a  conservative  phenomenon,  but  an 
evidence  of  failing  compensation,  has  been  pointed  out  by  Samways, 
who  in  36  severe  cases  of  mitral  stenosis  found  hypertrophy  in  26, 
whereas  dilatation  occurred  in  only  14,  in  11  of  which  it  was  asso- 
ciated with  hypertrophy.  This  process  of  dilatation  manifests 
itself  first  in  the  auricular  appendix,  owing  to  the  relatively 
unyielding  structures  by  which  the  auricle  proper  is  surrounded 
(the  aorta,  vertebrae,  and  esophagus  behind,  the  other  heart  cham- 
bers in  front,  the  diaphragm  and  liver  below,  and  the  aortic  arch 
and  pulmonary  artery  above).     (See  Figs.  45,  46,  and  47.) 

Thrombosis,  either  ante  mortem  or  post  mortem,  of  either  of 
these  chambers  occurs  frequently,  owing  to  circulatory  stagnation 
and  roughening  of  the  endocardium  bj^  vegetations.  (See  Fig.  9.) 
Such  a  state  of  affairs  is  a  prolific  source  of  emboli,  and  adds  much 
to  the  weakness  of  the  heart  which  is  manifest  during  intercurrent 
infections,   such  as  influenza,   and  which  is  often  attributed  to 

'  Hii'schfelder  and  Wolfsohn:  Johns  Hopkhis  Hosp.  Bulletin,  xix,  190S. 


:;-  —    to 


76  STUDIES   IN    CARDIAC    PATHOLOGY 

myocarditis  (Huchard).  Increased  pressure  leads  to  endocardial 
thickening  in  the  auricle,  and  as  compensation  fails,  to  thickening 
and  dilatation  of  the  pulmonary  arter3^  In  time  the  right  ven- 
tricle hypertrophies  as  the  result  of  pulmonary  stasis,  and  assumes 
a  somewhat  rectangular  shape  from  enlargement  of  the  conus. 
When  this  chamber  dilates  under  continuous  overstrain,  tricuspid 
insufficiency  occurs,  which  in  turn  leads  to  overdistention  of  the 
right  auricle.  This  chamber  in  extreme  cases  becomes  greatly 
thinned,  stretched,  and  ceases  to  contract,  becoming  eventually  a 
mere  distended  reservoir  at  the  orifices  of  the  venae  cavse. 

The  question  as  to  whether  mitral  stenosis  can  produce  left 
ventricular  hypertrophy  has  provoked  much  discussion,  a  good 
deal  of  which  may  be  found  in  Dunbar's  ^  article.  He  himself 
found  hypertrophy  and  dilatation  in  cases  with  good  compensa- 
tion. Some  observers  state  that  atrophy  is  the  corhmonest 
lesion,  and  attribute  its  existence  to  a  lessened  amount  of  blood 
which  this  chamber  is  called  upon  to  handle.  The  existence  of 
left  ventricular  hypertrophy,  when  present,  has  been  explained 
as  resulting  from  back  pressure  in  the  venous  system,  making- 
it  more  difficult  for  the  blood  to  pass  from  the  arteries  into  the 
veins,  and  thus  necessitating  increased  ventricular  effort.  An  in- 
creased systemic  venous  pressure  has  been  found  by  some  observers, 
but  is  denied  bj^  others.  Another  reason  for  hj^pertrophy  has 
been  offered  by  Giuffre,  namely,  that  diastolic  filling  is  interfered 
with  as  a  result  of  the  mitral  narrowing,  and  since  diastole  is  now 
generally  regarded  as  in  part,  at  least,  an  active  muscular  action, 
an  obstacle  to  it  would  lead  to  enlargement.  A  verj^  excellent 
study  of  this  subject  has  been  made  by  Hirsch,  who  examined  the 
hearts  in  ten  cases  by  the  Miillerian  method,  and  found  hyper- 
trophy only  when  insufficiency  of  the  mitral  was  the  chief  lesion. 
Schabert  also  found  either  an  actual  atrophy  of  the  ventricle  or 
at  least  no  increase  in  pure  obstruction.  There  seems  to  be  little 
doubt  that  left  ventricular  hypertrophy,  when  present,  can  generally 
be  accounted  for  by  other  lesions,  either  within  or  without  the  heart. 

'  Dunbar;  Dcut.  Arch.  f.  klin.  Med.,  1S92,  p.  283. 


DISEASES    OF   THE    MITRAL    ORIFICE  77 

Mitral  obstruction  may  be  produced  experimentally  either 
by  introducing  a  distensible  balloon  through  the  auricular  appen- 
dage, or  by  passing  a  suture  or  clamp  around  the  auriculo-ventric- 
ular  ring.^ 

"The  immediate  result  is  the  lowering  of  the  general  arterial  pressure  and 
the  great  elevation  of  the  pressure  in  the  pulmonary  arteries,  the  pulmonary 
veins,  and  the  left  auricle.  The  pressure  in  the  systemic  veins  is  little  if  at  all 
elevated,  unless  there  arises  an  insufficiency  of  the  right  ventricle,  or  with  it  a 
relative  insufficiency  of  the  tricuspid  valve.  The  essential  feature  of  the  process, 
as  indeed  of  all  changes  of  blood-pressure  due  to  any  obstruction  of  the  blood- 
stream from  alterations  of  the  heart,  lies  in  the  fact  that  the  amount  of  blood 
in  actual  circulation  is  diminished,  while  the  rest  of  the  blood  stagnates  behind 
the  obstruction." 

In  the  human  being  the  constrictive  process  occurs  gradually, 
and  thus  a  better  chance  for  compensation  is  offered.  The  fall 
in  the  systemic  pressure  is  counterbalanced  by  an  increased  arterial 
constriction,  so  that  arterial  tension  is  maintained  at  practically 
a  normal  level. 

Clinical  Considerations. — Owing  to  the  serious  and  progressive 
character  of  mitral  stenosis,  and  the  fact  that  so  manj'  cases  wreck 
individual  existences  early  in  life.  Sir  Lauder  Brunton  suggested 
some  years  ago  that  at  some  future  time  this  lesion  might  be 
treated  by  surgical  means.  At  present  this  is,  of  course,  out  of 
the  question,  but  recent  experience  shows  that  this  is  by  no  means 
as  chimerical  a  suggestion  as  it  at  first  appeared  to  be.  The 
heart  is  no  longer  surrounded  by  an  invincible  noli  me  tangere. 
Bernheim's  experiments  have  shown  that  it  is  a  good  deal  easier 
to  convert  a  mitral  obstruction  into  an  insufficiency  than  to  pro- 
duce the  former  lesion.^  Wounds  of  the  heart  are  treated  on  the 
same  principles  as  the  wounds  of  other  muscles,  and  with  no  small 
degree  of  success.  Of  some  160  cases  of  cardiac  wounds  surgically 
treated  thus  far,  69  were  in  the  right  ventricle,  with  48  deaths 
''69.6  per  cent.j;  74  in  the  left  ventricle,  with  45  deaths   (60.8 

'  Mlc.CMuu,  :iw\  .VInClurc;  'J'lvuis.  Assoc.  Am.  Phys.,  ]90(),  p.  5. 
■'  I5r-nilii-i,„:   l;,il|..tin  .lolms  llcpkiiis  Ilospiliil,  April,  HIOO. 


78  STUDIES   IN    CARDIAC    PATHOLOGY 

per  cent.);  5  in  the  left  auricle,  with  2  deaths  (33.3  per  cent.).^ 
Furthermore,  Elsberg-  has  shown  experimentally  that  the  heart 
in  rabbits  and  dogs  is  capable  of  resisting  an  astonishing  amount 
of  trauma,  "even  ligation  of  the  entire  left  heart  at  the  junction 
of  the  lower  and  middle  thirds  of  the  ventricles,  and  amputation 
through  the  ventricles  below  the  ligature,  may  be  followed  by 
recovery." 

While  mitral  stenosis  is  generally  and  justly  regarded  as  a 
far  more  serious  lesion  than  insufficiency,  yet  this  question  is 
worthy  of  some  little  thought.  Mitral  stenosis  is  perhaps  not  so 
rare  a  lesion  as  some  of  us  think,  ^  and  the  recent  investigations 
of  Schabert  are  at  least  suggestive  of  the  fact  that  some  stenoses 
may  be  the  terminal  stages  of  insufficiencies.  The  question  as 
to  the  preponderance  of  the  lesion  can  to  a  certain  extent  be 
determined  by  careful  weighing  of  the  fat-  and  blood-freed  in- 
dividual heart  chambers,  and  by  the  water  test;  but,  needless 
to  say,  other  conditions,  such  as  the  hypertension  of  nephritis, 
must  be  carefully  excluded  before  drawing  definite  conclusions. 

The  fact  that  mitral  obstruction  is  not  rarely  associated  with 
congenital  malformations  naturally  suggests  a  common  cause, 
such  as  syphilis,  alcoholism,  tuberculosis  in  the  parents,  etc. 
Heitz  and  Lezary*  have  recently  collected  15  cases  in  which,  in 
addition  to  mitral  stenosis,  such  lesions  as  syndactjdia,  ectopic 
testicles,  harelip,  sternal  malformations,  imbecility,  were  observed. 
It  is  quite  possible,  however,  that  such  cases  are  coincidences, 
or  the  result  of  an  intrauterine  infection,  since  the  symptoms  of 
mitral  stenosis  rarely  manifest  themselves  before  the  twelfth 
year  (Poynton).  A  "mitral  heredity"  has  been  dwelt  upon  by 
Hirtz.'^ 

'  Peck:  Annals  of  Surgery,  July,  1909. 
■-  Elsberg:  Jour.  Exper.  Med.,  1899,  p.  479. 

'  Cabot  states  that  2.5  out  of  48  cases  discovered  at.  autopsy  at  the  Massachusetts  General 
Hospital  were  overlooked  clinically. 

*  Heitz  and  Lezary:  Arch.  d.  Mai.  du  Cccur,  190S,  i,  p.  701. 
^Hirtz:  Presse  Med.,  Sept.  19,  1903. 


Tic.  24. — Stenosis  of  the  Aortic,  Mitral,  and  Tricuspid  Valves. 

The  aortic  leaflets  are  fused  together  and  the  orifice  is  greatly  reduced  in  caliber.  The 
mitral  orifice  consists  of  a  mere  .slit,  of  crescentic  outline — buttonhole  type.  The  tricuspid 
orifice  is  also  contracted.     (Specimen  from  the  Philadelphia  Hospital.) 


80  STUDIES   IN    CARDIAC    PATHOLOGY 

MITRAL  INSUFFICIENCY 

Pathogenesis. — The  mitral  valves  may  fail  to  prevent  back- 
ward leakage  owing  to  organic  disease  or  to  atonicity  of  the  mus- 
cular sphincter,  upon  the  integrity  of  which  the  proper  functiona- 
tion  of  the  valve  so  largely  depends.  This  atonicity  of  the  sphinc- 
ter in  turn  may  result  from  muscular  degeneration  or  from  purely 
functional  causes.  The  conditions  necessary  to  produce  a  func- 
tional lesion  are  diminished  muscular  tonicity  and  an  overworked 
ventricle.  When  mitral  insufficiency  results  from  organic  causes, 
it  is  not  infrequently  associated  with  some  obstruction.  The 
valves  may  be  fused,  retracted,  puckered  together  with  more  or 
less  induration  of  the  leaflets  or  the  surrounding  structures. 
Insufficiency  may  also  occur  when  the  left  ventricle  enlarges  to 
such  an  extent  as  to  draw  on  the  papillary  muscles  before  the 
leaflets  are  in  complete  apposition.  Actual  ulcerations,  perfora- 
tions, or  vegetations  may  also  prevent  sufficiency.  In  fact, 
Schabert's  recent  studies  indicate  that  such  lesions  are  the  com- 
monest cause  of  pure  organic  mitral  insufficiency. 

Occurrence. — Mitral  insufficiency  is  the  commonest  of  all 
valvular  diseases,  constituting  about  25  per  cent,  of  all  such  cases. 
Among  1,024  cases  of  valvular  disease  in  applicants  for  life  in- 
surance Ashton  found  mitral  stenosis  32,  insufficiency  557,  aortic 
obstruction  136  (?),  insufficiency  47.^  At  the  Edinburgh  Infirmary 
out  of  1,914  cases  of  valvular  disease  there  were  585  cases  of  pure 
insufficiency,  and  463  combined  mitral  lesions,  231  of  which  were 
mitral  stenoses.^  Among  the  8,640  autopsies  at  the  Phila- 
delphia General  Hospital  there  were  1,253  cases  of  chronic  mitral 
endocarditis.  Among  these  there  was  one  aneurism  (with  rupture), 
one  hematoma,  and  one  case  of  supernumerary  leaflets. 

The  great  discrepancy  between  the  frequency  of  the  diagnosis 
of  mitral  insufficiency  in  clinical  records,  and  in  autopsy  statistics, 
is  to  be  explained  by  the  fact  that,  accepting  the  statement  of 

1  Ashton:   Medical  News,  June  .30,  1894. 

^  Gillespie:  Edinburgh  Hospital  Reports,  1S9S,  p.  31. 


DISEASES    OF   THE    MITRAL    ORIFICE  81 

Virchow,  it  has  been  held  to  be  impossible  to  test  the  functionation 
of  this  valve  by  hydrostatic  methods,  in  the  way  in  which  the 
semilunar  valves  may  be.  Lately  Schabert  ^  has  especially  studied 
this  question  and  found  that  such  a  test  can  be  made  with  com- 
parative satisfaction,  celerity,  and  accuracy,  and  as  a  result  three 
grades  of  insufficiency  have  been  suggested.  (The  valves  may 
also  be  tested  with  an  air-bellows.-) 

The  left  auricle  is  cut  up  as  far  as  the  mitral  insertion,  and  the  flap  reflected 
for  inspection.  The  aorta  is  occluded  by  pinching,  and  through  a  cut  in  the 
ventricular  wall  a  tube  connected  with  running  water  is  introduced  into  the 
ventricle.  A  source  of  error  is  admitted  for  hearts  of  greatly  relaxed  muscula- 
ture,— anemia,  sepsis,  postmortem  decomposition,  etc., — and  also  for  cases  in 
which  thrombi  are  lodged  between  the  leaflets.  Similar  conclusions,  though 
based  on  a  different  technic,  have  been  reached  by  Oesterreich  and  Bleicheroeder.^ 

Notwithstanding  these  tests,  however,  functional  and  even 
organic  insufficiency  is  often  overlooked  at  autopsy  on  account 
of  rigor  mortis  of  the  heart  muscle  which  prevents  relaxation, 
and  also  on  account  of  the  redundancy  of  the  valves. 

Pathologic  Anatomy. — The  anatomic  changes  in  mitral  in- 
sufficiencjf  consist  of  sclerotic,  ulcerative,  or  vegetative  alterations 
of  the  leaflets  or  chordae  tendinese,  with  occasional  perforation  or 
rupture,  and  frequently  with  induration  and  shortening.  The 
commonest  sign  of  relative  insufficiency  consists  of  thickening  of 
the  free  valvular  margin  with  more  or  less  contraction,  the  former 
being  generally  uniform.  Inversion  of  the  flaps  is  rare  because 
the  chordae  tendinese  are  so  attached  as  to  leave  a  considerable 
margin  between  their  insertions.  When  actual  inversion  does 
occur,  it  is  generally  on  the  anterior  leaflet.  On  the  posterior 
surface  of  the  auricle,  between  the  valve  opening  and  the  mouth 
of  the  pulmonary  veins,  we  sometimes  find  the  endocardium 
infiltrated  and  thickened,  presenting  an  angular,  ridgy,  gelatinous 
appearance,    with    the    convexity    toward    the    pulmonary   veins 

'  Schabert:  Zontralb.  f.  Path.  u.  path.  Anat.,  1907,  p.  3.3. 
'  Hamilton:  Tc.xt  Hook  of  P.ath.,  1889,  p.  9. 

'  Oostfrrcich  aud  HIcichcrocclcr:   Virfhow's  Arch,,  vol.  cli,  p.  19.5,  1902,  p.  l.'J9. 
6 


82  STUDIES  IN  CARDIAC  PATHOLOGY 

(Zahn).  In  the  earlier  stages  the  auricle  is  hypertrophied,  and 
in  advanced  cases  atrophied.  The  valvular  leaflets  are  thickened 
and  at  times  show  aneurismal  dilatation.  (See  Fig.  15.)  The 
auricular  surface  of  the  anterior  leaflet  generally  shows  the  most 
marked  changes.  The  early  evidences  of  rheumatic  endocarditis 
consist  of  small  nodules  on  the  leaflets,  and  are  of  little  importance 
of  themselves.  The  later  and  serious  changes  result  from  extension 
of  the  inflammatory  process  to  the  chordae  tendinese,  which  become 
thickened  and  shortened.  "Rheumatic  disease  of  the  mitral 
valve  is  mainly  a  disease  of  the  chordae  tendinese"  (Fisher). 
This  process  of  contraction  ultimately  leads  to  stenosis  and  in- 
sufficiency. 

Pathologic  Physiology. — "In  every  variety  of  uncompensated 
valvular  lesion,  either  an  insufficiency  or  an  obstruction,  blood- 
pressure  and  systolic  output  fall  on  the  distal,  and  rise  on  the 
proximal,  side  of  the  lesion.  Compensation  is  brought  about  by 
transferring  backward  to  another  heart  chamber  the  increased 
pressure.  Compensation  is  brought  about  in  the  stenoses  by 
increased  contractile  tension,  and  in  the  insufficiencies  by  increased 
systolic  output.  As  a  corollary,  to  compensate  an  obstruction 
hypertrophy  is  required,  but  to  compensate  an  insufficiencj'^,  both 
hypertrophy  and  dilatation  must  exist"  (Moritz).^  As  the 
result  of  mitral  insufficiencj'',  pressure  in  the  aorta  falls,  in  the  pul- 
monary veins  and  in  the  arteries  it  rises,  wherefore  the  amount  of 
blood  in  the  greater  circulation  diminishes;  in  the  lesser,  increases. 
The  systolic  output  of  the  left  ventricle  increases,  that  of  the 
right  decreases.  Distinct  dilatation  of  the  right  ventricle  is  not 
the  result  of  pure  mitral  insufficiency.  Mitral  insufficiency  leads 
to  dilatation  and  hypertrophy  of  the  left  ventricle.  With  increase 
of  left  ventricular  systolic  output,  the  aortic  pressure  may  return 
to  normal  and  the  pulmonic  pressure  diminish  to  normal;  true 
compensation  is,  therefore,  possible.  In  mitral  stenosis  the  work 
of  the  left  ventricle  decreases. 

1  Moritz:   Deut.  Arch.  f.  klin.  Med.,  1899,  Ixvi,  p.  349. 


Fig. 


-Mitral  Insufficie.ncy. 


ShowinK  vr-ry  extensive  tissue  destruction.  The  chorda;  tendineaj  at  the  central  part  of 
the  valvular  margin  have  been  destroyed  by  ulceration,  leaving  only  short  shriveled  stumps. 
A  few  vorruco.se  vegetations  are  seen.  The  ventricular  wall  is  much  thickened.  (Specimen 
from  the  Pennsylvania  Hospital.) 


84  STUDIES  IN  CARDIAC  PATHOLOGY 

When  mitral  insufficiency  is  exj)erimentally  produced — by 
cutting  the  leaflets  or  chordee  tendinese  by  means  of  a  knife-hook 
introduced  through  the  left  auricular  appendage — arterial  pressure 
falls  in  proportion  to  the  severity  of  the  lesion.  Pressure  in  the 
pulmonary  artery  is  not  much  altered;  it  falls  somewhat,  with 
extreme  insufficiency,  and  with  slight  lesions  rises  somewhat. 
The  systemic  venous  pressure  too  shows  but  little  change.  The 
most  striking  alterations  occur  in  the  left  auricle,  in  which  pressure 
rises,  distention  becomes  marked,  and  the  pulsation  not  only 
violent,  but  systolic  in  time.  The  latter  occurs  because  the 
auricle  now  forms  practically  a  continuous  chamber  with  the 
ventricle,  and  the  powerful  contraction  of  the  latter  far  over- 
shadows the  feeble  pulsation  of  the  former.  Mitral  insufficiency 
brings  about  hypertrophy  and  later  dilatation  of  the  left  auricle. 
The  greater  the  leakage,  the  greater  the  dilatation.  When 
regurgitation  is  less  extreme,  there  is  apt  to  be  more  hypertrophy 
(Gibson). 

Hypertrophy  of  the  left  ventricle  occurs  on  account  of  the 
increased  amount  of  blood  which  this  chamber  has  to  handle  in 
order  to  keep  up  anj'thing  like  a  normal  circulation.  But  since 
this  merel}^  means  that  a  certain  amount  of  blood  is  forced  back 
against  the  lower  auricular  pressure,  it  is  more  likely  that  the 
ventricle  actually  does  less  and  not  more  work  than  normal. 
When  marked  hypertrophy  is  present,  in  such  cases,  it  is  often  due 
to  other  causes,  such  as  arteriosclerosis,  etc.  Congestion  of  the 
lungs  generally  occurs  sooner  or  later,  and  this  is  followed  bj^  a 
train  of  changes  similar  to  that  described  under  mitral  stenosis. 
Thrombosis  of  the  cavities  is  common  in  the  later  stages,  both  as 
an  antemortem  and  as  a  postmortem  occurrence.  Left  ventricular 
dilatation  enables  the  ventricle  to  receive  the  increased  amount 
of  blood  which  is  furnished  first  by  increased  auricular  activity, 
and  later  by  right  ventricular  hypertrophy. 

The  cause  of  the  right  ventricular  hypertrophy  has  been  much 
discussed.     The  experiments  of  MacCallum  and  McClure  have 


DISEASES    OF   THE    MITRAL    ORIFICE  85 

shown  that  in  so  far  as  blood-pressure  changes  are  an  index, 
the  pulmonary  capillaries  may  be  regarded  as  a  system  of  rigid 
tubes,  and  inasmuch  as  the  left  ventricular  contractions  are  trans- 
mitted backward  into  the  pulmonary  artery  with  so  little  loss  of 
time,  the  contraction  of  the  left  ventricle  is  manifested  in  the  right 
ventricle  during  the  systole  of  the  latter.  An  additional  cause  for 
right  ventricular  hypertrophy  lies  in  the  fact  that  when  the  left 
auricle  becomes  dilated,  as  it  early  does,  it  compresses  the  upper 
left  pulmonary  vein  between  the  auricular  appendix  and  the 
bronchus;  left  ventricular  enlargement  tends  to  compress  the 
left  lower  pulmonary  vein,  while  right  auricular  enlargement 
encroaches  upon  the  right  pulmonary  veins.  Compression  of 
these  veins  at  once  produces  congestion  in  the  arterial  and  venous 
radicles  of  the  lungs  and  pleurae.     (See  Fig.  45.) 

Right-sided  cardiac  hydrothorax  or  pulmonary  congestion 
often  occurs  without  evidences  of  stasis  in  the  greater  circulation, 
and,  when  present,  the  hydrothorax  is  generally  confined  to,  or 
most  marked  on,  the  right  side.  This  right-sided  localization, 
which  was  formerly  attributed  to  pressure  by  the  dilated  auricle 
upon  the  vena  azygos  major,  has  been  shown  by  Fetterolf  and 
Landis  ^  to  be  the  result  of  right  auricular  pressure  upon  the  pul- 
monarj^  veins,  into  which  the  vessels  of  the  pleura  empty.  Pressure 
on  the  vena  azygos  major  by  the  dilated  right  auricle  is  anato- 
micalh^  impossible.  Marked  dilatation  of  the  left  coronary  sinus 
has  simulated  an  enormously  dilated  right  auricle,  seemingly 
overlapping  the  left  auricle  from  behind.- 

"The  greater  frequency  of  hydrothorax  on  the  right  side  is  due  to  the  fact 
that  dilatation  of  the  right  auricle  is  more  common  and  more  easy  than  a  similar 
condition  on  the  left  side,  and  such  dilatation  is  the  only  factor  needed  to  cause 
damming  back  in  the  right  pulmonary  veins.  On  the  left  side  in  order  to  include 
both  uf)per  and  lower  veins  there  is  needed  dilatation  of  the  left  auricular  appen- 
dix and  the  left  ventricle,  with  possibly  a  retrodisplacement  of  the  vertical 
septum"  f Fetterolf  and  Landis). 

'  Fr;t,U;rolf  and  Landi.s:  Am.  .lour.  Mod.  Soi.,  Nov.,  1909,  p.  712. 
Miollct:   Wion.  klin.  VVndi.,  1910,  |,.  119, 


V.  DISEASES  OF  THE  TRICUSPID  ORIFICE 

Pathogenesis. — Valvular  disease  of  the  right  heart  is  much 
less  common  than  of  the  left.  This  apparently  bears  some  relation 
to  the  much  greater  work  which  the  left  heart  has  to  perform, 
since  during  fetal  life,  when  this  difference  does  not  exist,  the 
proportionate  involvement  of  the  two  sides  is  about  equal.  Two 
facts  which  recent  investigations  seem  to  have  emphasized  are 
that  tricuspid  disease,  while  by  no  means  common,  is  not  so  rare 
as  has  hitherto  been  supposed,  and  that  when  present  it  is  more 
frequently  the  result  of  acquired  disease  than  of  a  congenital 
defect.  This  statement,  of  course,  refers  only  to  actual  organic 
disease  of  the  valve,  and  not  to  simple  atonic  dilatation  of  the 
orifice,  which  is  very  common.  The  functional  efficiency  of  this 
valve  depends  very  largely  upon  the  tone  of  the  sphincter-like 
muscular  fibers  surrounding  the  orifice.  Both  Harvej^  and  Hunter 
realized  that  the  tricuspid  valve  is  a  much  less  perfect  valvular 
mechanism  than  the  mitral.  We  are  not  surprised  to  find,  there- 
fore, that  tricuspid  stenosis  is  one  of  the  rarest,  and  tricuspid 
insufficiency  one  of  the  commonest,  valvular  lesions. 

Griffith,'  in  an  excellent  study  of  270  cases  of  tricuspid  disease,  in  which 
simple  dilatation  was  excluded,  has  called  attention  to  the  foregoing  facts. 
Among  150  specimens  of  cardiac  disease  in  the  Pathological  Museum  of  York- 
shire College  studied  by  him,  there  were  no  less  than  26  instances  of  organic 
tricuspid  disease,  all  of  which  were  apparently  acquired  after  birth.  Fenwick  - 
and  Herrick  ^  have  arrived  at  similar  conclusions.  The  latter  among  154  cases  of 
tricuspid  stenosis  found  an  antecedent  rheumatic  history  in  57,  probable  rheu- 
matism in  4,  chorea  in  2.  Among  28  there  was  no  such  history,  and  in  the  re- 
mainder the  etiologic  factor  could  not  be  determined.  Combining  the  statistics 
of  Leudet,''  Herrick,  and  Griffiths,  there  was  a  history  of  rheumatic  fever  or 

1  T.  W.  Griffith;  Edinburgh  Med.  Jour.,  1903,  Iv,  105. 
-Fenwick:   Transactions  Pathological  Society  of  London,   ISSl. 
'  Herrick:  Boston  Med.  and  Surg.  Jour.,  1S97,  cxxxvi,  2-15. 
"Leudet:  Paris  Thesis,  1881. 


DISEASES    OF   THE    TRICUSPID    ORIFICE  87 

chorea  in  34.9  per  cent.     Pitt's  ^  series  showed  a  percentage  of  62,  due  to  these 
causes. 

Tricuspid  stenosis  is  nearly  always  associated  with  other  valvular  lesions, 
especially  mitral  stenosis,  as  the  collected  statistics  of  Herrick  show. 

Tricuspid  and  mitral  stenosis 102 

Tricuspid  stenosis  alone 14 

Tricuspid  and  pulmonary 1 

Tricuspid,  aortic,  and  pulmonary 2 

Tricuspid  and  aortic 64 

Tricuspid  and  mural 1 

184 

In  only  6  of  the  last-named  author's  cases  was  there  not  also  some  mitral 
involvement,  and  in  only  4  cases  were  all  the  other  valves  normal.  The  Guy's 
Hospital  material  collected  by  Pitt  showed  only  2  among  87  cases  without  coin- 
cident mitral  stenosis.  These  facts  alone  point  very  strongly  toward  an  in- 
flammatory origin,  although  they  have  been  used  in  explaining  the  tricuspid 
stenosis  as  the  result  of  back  pressure  from  mitral  obstruction.  But  such  a 
result  does  not  follow  mitral  insufficiency  in  which  there  is  also  back  pressure, 
and,  furthermore,  actual  endocarditic  vegetations  are  not  infrequently  found  on 
the  tricuspid  valve.  However,  some  recent  investigations  have  tended  to 
corroborate  the  back  pressure  theory.  "In  view  of  the  work  of  Goodhart,  Roy 
and  Adami,  and  Weber  and  Deguy,  it  is  not  unlikely  that  the  overstrain  of  the 
right  ventricle  leads  to  edema  and  hemorrhage  into  the  tricuspid  valve,  and  that 
these  processes  usher  in  the  fibrosis.  In  other  words,  the  mitral  lesion  itself 
becomes  an  etiologic  factor  in  the  tricuspid  lesion,  and  the  pathologic  process 
completed  in  the  mitral  is  now  transferred  one  step  back  in  the  circulation  and 
repeats  itself  in  the  tricuspid"  (Hirschfelder). 


TRICUSPID  OBSTRUCTION 

Occurrence. — At  the  Philadelphia  General  Hospital  among 
8,640  autopsies  there  were  162  cases  of  chronic  tricuspid  endocard- 
itis. There  were  58  instances  of  marked  incompetence,  8  cases 
of  stenosis,  4  cases  of  marked  calcification,  and  1  case  of  super- 
numerary leaflets.  Tricuspid  obstruction  is  much  commoner 
in  women  than  in  men  (133  to  38)  and  between  the  second  and 
third  decades  (Herrick). 

Occasionally  tricuspid  obstruction  has  a  congenital  origin. 
Some  cases  show  a  nodular  condition  of  the  valves  near  their 
margins.     In  the  fetus  the  blood-vessels  extend  nearer  to  the  free 

'  Pitt:  Allbutt's  Sy.stom  of  Medicine,  vol.  i. 


85  STUDIES  IN  CARDIAC  PATHOLOGY 

margins  than  in  the  adult  (Darier),  and  as  thej^  retract  small 
areas  may  remain,  which  may  cause  hematomas.  Rarely  ob- 
struction may  be  caused  by  tumors  or  ball  thrombi  (Gairdner). 
Morbid  Anatomy. — From  what  has  just  been  said  it  will  be 
evident  that  the  condition  of  the  heart  will  vary  according  to 
the  time  at  which  death  occurred.  During  the  first  stage  there 
will  be  a  hj'pertrophic  enlargement  of  the  auricular  wall  and  of 
the  superior  vena  cava.  During  the  second  stage  the  caval 
orifice  is  found  greatly  enlarged,  so  that  the  auricle  and  the  veins 
form  a  continuous  sac.  Thus,  in  one  case  a  thrombus  was  found 
which  extended  from  the  auricle  directly  backward  into  the  cervical 
vessels.  The  auricular  myocardium  in  such  cases  undergoes 
atrophy  and  may  become  almost  a  mere  fibrous  sac  formed  by 
the  endocardium  and  epicardium.  Pericarditis,  sometimes  acute, 
but  more  frequently  the  chronic  adhesive  variety,  has  been  found 

Fig.  26. — Acute  and  Chronic  Endocarditis,  Mitral  Stenosis. 

A.  L.,  white,  laborer,  aged  forty-two  years.  (Philadelphia  Hospital,  vol.  xviii,  p.  210. 
Physician:  Dr.  S.  S.  Cohen.     Pathologist:  Dr.  Funke.) 

Clinical  Notes:  Was  admitted  complaining  of  cough,  anasarca,  and  dyspnea.  The 
latter  had  existed  for  two  years. 

Physical  Examination:  Heart:  The  apex-beat  extends  from  the  fifth  to  the  eighth 
interspaces  in  the  anterior  axillary  line.  There  is  no  thrill.  The  dullness  extends  from  the 
mid-sternal  to  the  anterior  axillary  lines.  A  presystolic  murmur  is  heard  near  the  apex  when 
the  heart  beats  strongly.  The  first  sound  is  loud  and  booming,  and  followed  by  a  soft  systolic 
murmur  which  is  transmitted  to  the  axilla,  at  which  point  it  is  loudest.  The  aortic  second 
sound  is  feeble,  the  pulmonic  second  accentuated,  and  the  heart  action  tumultuous.  A  sys- 
tolic murmur  is  also  heard  at  the  aortic  and  at  the  tricuspid  area. 

The  patient  improved  under  treatment  until  he  was  able  to  leave  his  bed  for  half  an  hour. 
On  the  second  day  of  his  so  doing  he  suddenly  fell  to  the  floor,  greatly  cyanosed,  and  died  almost 
at  once. 

Pathologic  Di.^gnosis:  Acute  and  chronic  endocarditis,  mitral  stenosis,  pulmonary  in- 
farction (anemic),  renal  congestio7i. 

Heart:  Weighs  500  gm.  The  right  side  is  dilated,  its  muscle  thin,  bright  red  in  color, 
and  its  endocardium  opaque.  The  foramen  ovale  is  obliquely  patulous.  The  tricuspid  orifice 
admits  three  fingers  with  ease.  The  right  ventricular  wall  measures  0.5  cm.;  it  is  quite  firm, 
and  traversed  by  yellowish  lines  which  commence  in  the  subpericardial  fat.  The  papillary 
muscles  are  firm,  and  bright  red  in  color.  One  of  the  mitral  leaflets  contains  two  fenestrations 
along  its  line  of  contact.  The  pulmonary  leaflets  are  normal.  The  left  auricle  is  distended, 
thin,  pale,  and  its  endocardium  opaque.  The  mitral  orifice  barely  adm,its  one  finger.  The  left 
ventricle  is  large  and  contains  several  post-mortem  clots,  and  measures  2.5  cm.  at  its  thickest  point, 
its  muscle  being  firm  and  pale.  The  mitral  leaflets  are  thickened,  shortened,  and  adherent, 
especially  at  the  inner  angle.  On  the  posterior  surface  are  numerous  small,  pendulous,  pinkish 
vegetations,  about  4  mm.  in  length,  which  are  adherent  to  the  leaflets.  The  aortic  leaflets  are 
slightly  thickened,  especially  at  their  bases. 


Fig.  26. 


90  STUDIES  IN  CARDIAC  PATHOLOGY 

with  somewhat  astonishing  frequency.  In  so  far  as  the  valves 
are  concerned  the  structural  changes  which  have  been  noted 
are  practically  those  which  are  met  with  in  other  varieties  of 
endocarditis — vegetations,  sclerosis,  changes  in  the  chordse 
tendinese,  papillary  muscles,  etc.  (See  Figs.  23,  24,  28.)  In  two 
instances  pedunculated  tumors  have  been  reported.  Perhaps  the 
most  frequent  finding  has  been  a  fusion  of  the  valvular  curtains, 
producing  a  funnel-shaped  stenosis.  The  degree  of  the  latter, 
of  course,  varies  with  the  case.  In  the  older  writings  several 
references  are  made  to  the  case  of  General  Wipple,  reported  by 
Corvisart,  in  which  the  valves  were  so  extensively  calcified  that 
only  a  small  slit-like  opening  remained. 

Recent  vegetations,  even  when  of  considerable  size,  are  more 
apt  to  produce  an  insufficiency  than  a  stenosis.  Such  high  degrees 
of  contraction  as  are  met  with  in  mitral  disease  are  very  rarely 
found,  and  nearly  always  the  aperture  will  admit  two  fingers. 
The  crescentic  slit  so  common  in  mitral  stenosis  is  rarely  found 
on  the  right  side  of  the  heart,  whereas  calcification  seems  to  be 
much  more  common  (Crawford).^ 

Inasmuch  as  the  congenital  variety  of  tricuspid  stenosis  is,  so 
far  as  we  can  judge,  generally  the  result  of  a  fetal  endocarditis, 
it  is  not  surprising  that  the  pathologic  appearance  presents  no 
especial  features  distinguishing  it  from  the  post-natal  form.  It 
may,  however,  be  due  to  true  malformation  and  be  associated 
with  other  anomalies,  such  as  a  persistent  ductus  arteriosus,  im- 
perforate ventricular  septum,  patulous  foramen  ovale,  etc. 

Before  closing  this  section,  attention  should  be  called  to  the 
fact  that,  owing  to  the  almost  constant  association  of  tricuspid 
and  mitral  stenosis,  it  is  often  very  difficult  to  determine  how 
much  or  how  little  effect  the  latter  has  had  in  bringing  about 
the  secondary  changes  in  the  heart. 

(Figs.  15,  20b,  23,  and  24  were  from  cases  of  combined  lesions; 
in  the  first,  at  least,  there  was  a  definite  history  of  rheumatic  fever 

'  R.  Crawford:  Practitioner,  1907,  Ixxviii,  191. 


Fk;.  27. — Chronic  Mitral  Endocarditis. 

Female,  white,  aged  forty-three  years.  (Pennsylvania  Hospital.  Autopsy  No.  309. 
Pathologist:  Dr.  Longcope.) 

Clinical  Notes:  Past  history  negative.  For  the  last  six  weeks  has  had  abdominal 
swelling,  post-prandial  discomfort,  slight  loss  of  weight,  and  some  edema  of  the  feet. 

A  systolic  murmur  is  heard  at  the  aortic  area  which  is  transmitted  down  the  sternum. 
There  is  also  a  systolic  thrill.  Ascites  is  present.  Paracentesis  abdominalis  was  twice  per- 
formed.    Death  occurred  gradually,  with  the  symptoms  of  peritonitis. 

Pathologic  Diagnosis:  Carcinomatosis  of  the  peritoneum,  etc.  Chronic  mitral  endo- 
carditis.    Fatty  degeneration  of  the  heart,  etc. 

Pericardiu.m:  Contains  100  c.c.  of  clear  fluid.     It  shows  no  abnormalities. 

Heart;  Is  not  increased  in  size;  it  weighs  240  gra.,  and  contains  fluid  blood  and  a  few 
postmortem  clots.  The  epicardium  contains  much  fat;  it  is  smooth  and  glistening  and  its 
ve.s.sels  are  not  especially  prominent.  The  heart  muscle  is  of  a  pale  yellowish-brown  color, 
and  shows  yoUowi.sh  flecking  beneath  the  endocardium  of  the  left  ventricle,  which  is  12  to  15 
ram.  in  thickness.  Tricuspid  and  pulmonary  valves  are  normal.  The  mitral  valve  is  thickened 
along  its  free  edqes,  the  leaflets  are  slightly  retracted,  and  the  chordm  tendine(E  are  distinctly  short- 
ened. The  aortic  valves  are  thickened,  not  retracted;  the  corpora?  Arantii  are  knobbed.  The 
aorta  show.s  moderate  sclerosis,  in  irregular  plaques,  and  one  or  more  calcified  plates.  The 
coronary  arteries  are  patent  and  smooth.     The  auricular  appendages  are  free  from  thrombi. 


92  STUDIES  IN  CAKDIAC  PATHOLOGY 

four  years  before  death.)  The  diagnosis  is,  therefore,  obviously 
often  overshadowed  bj^  the  associated  mitral  lesion.  In  the  few 
cases  of  isolated  tricuspid  stenosis  which  have  been  reported, 
the  diagnosis  of  mitral  stenosis  was  generally  made,  although 
there  have  been  several  cases  in  which  the  condition  has  been 
correctly  recognized  intra  vitam,  beginning  with  Gairdner's  case 
in  1862.' 

Pathologic  Physiology. — In  case  of  obstruction  of  the  tricuspid 
orifice  the  right  ventricle  is  filled  more  slowly  than  normal,  and 
the  right  auricle  hypertrophies.  When  the  stenosis  increases 
or  the  nutrient  blood-supply  fails  to  meet  the  unusual  demands, 
dilatation  follows.  Clinically  this  is  well  illustrated  in  the  char- 
acter of  the  venous  pulse.  During  the  first  stage  the  auricular 
(presystolic)  wave  is  large  and  well  marked;  during  the  second 
stage,  when  the  auricle  becomes  overdistended  and  paralyzed, 
the  veins  remain  permanentlj^  full  and  cease  to  pulsate.  At 
first  the  venous  regurgitation  into  the  cavse  is  prevented  by  a 
hypertrophy  of  the  tenia  terminalis  and  the  other  fibers  which 
tend  to  close  the  caval  orifice  of  the  auricle  during  its  systole. 
Later,  stasis  and  congestion  of  the  portal  sj^stem,  etc.,  follows. 
(See  Fig.  46.) 

TRICUSPID  INSUFFICIENCY 

Pathologic  Anatomy. — The  leaflets  are  generally  elongated  and 
thinned,  while  the  free  margins  are  thickened  and  (contrary  to 
mitral  insufficiency)  everted.  The  thickened  portion  may  be 
soft  or  indurated,  and  not  rarely  on  its  auricular  surface  shows 
localized  loss  of  tissue,  resembling  ulceration.  (This  occurred 
in  17  of  Sierro's  -  38  cases.)  These  changes  occur  oftenest  on 
the  free  margin  of  the  middle  leaflet,  with  the  anterior  leaflet 
next  in  frequenc3^  The  chordae  tendinese  are  often  attenuated 
and  elongated,  and  the  tip  of  the  papillary  muscle  not  infrequently 
is  indurated.     The  tricuspid  opening  is  enlarged.     There  is  also 

1  Gairdner:  Clinical  Medicine,  1862,  p.  602. 

2  Sierro :  Contribution  a  lY'tude  des  ulcer,  chron.  dc  la  valvule  tricuspide,  These  de  Geneve, 
1886. 


Fio. 


•Ar't-fE   AND  Chronic  Endocarditis  of  the   Aortic,   Mitral, 
Valves. 


AND  Tricuspid 


The  uppfT  portion  of  the  auricles  has  been  cut  away.  The  three  valvular  orifices  thus 
e.'cpo.sed  show  induration  and  contraction  of  their  component  tissues.  The  mitral  valve  in 
nrldition  shows  a  Larue  dark  mass  of  vegetations  of  recent  origin  which  almost  completely 
occlude  its  orifice.  The  endocardium  and  myocardium  of  1)(](  h  auricles  are  t  hickened.  (Photo- 
graph by  Dr.  Alfred  II.  Allen.) 


94  STUDIES    IN    CARDIAC    PATHOLOGY 

a  diffuse  thickening  of  the  endocardium  of  the  right  auricle.  The 
right  auricular  appendix  is  dilated  and  the  fossa  ovalis  depressed. 
In  cases  in  which  the  foramen  ovale  is  patent,  the  surrounding 
endocardium  is  additionally  thickened.  The  auricular  muscle 
is  at  times  hypertrophied,  again  seemingly  attenuated  (Zahn). 

Pathologic  Physiology. — Stadler  ^  has  produced  tricuspid  in- 
sufficiency experi'mentalhj  in  rabbits.  The  animals  lived  several 
weeks  (nine  to  one  hundred  and  seventy-six  days),  and  developed 
ascites,  edema,  and  hepatic  enlargement.  The  hearts  were 
examined  by  Miiller's  method  and  showed  distinct  hypertrophy 
of  the  right  auricle  and  ventricle,  but  in  some  marked  cases 
atrophy  of  the  left  ventricle  occurred,  due  apparently  to  the 
smaller  amount  of  blood  handled.  In  the  less  severe  lesions  this 
did  not  occur,  from  which  it  appears  that  even  tricuspid  insuffi- 
ciency may  be  compensated  by  increased  vascular  tone  and  hyper- 
trophy of  the  right  auricle,  which  not  only  contracts  more  forcibly 
but  aspirates  blood  from  the  veins  more  powerfully. 

Both  the  heart  and  the  vense  cavte  play  an  important  role  in 
maintaining  compensation  in  tricuspid  insufficiency.  By  virtue 
of  the  increased  venous  pressure  the  right  ventricle  may  be  said 
to  contract  against  a  wall  of  blood  which  helps  to  prevent  re- 
gurgitation. Again,  this  increased  venous  pressure  causes  a 
rapid  filling  of  the  chamber  during  diastole. 

Franke  has  called  especial  attention  to  the  role  of  the  liver. 
Inasmuch  as  all  cases  of  tricuspid  insufficiency  are  not  accompanied 
by  ascites,  and  since  neither  suction  of  the  right  heart  nor  elasticity 
of  the  venaj  cavse  are  sufficient  to  explain  its  non-occurrence,  we 
must  assume  that  the  liver  plays  an  important  role.  During 
systole  venous  blood  is  actually  forced  out  of  the  hepatic  cells 
into  the  portal  system,  by  the  higher  pressure  which  exists  in 
the  arterial  system.-     (See  Fig.  46.) 

Of  course,  this  really  means  that  the  left  ventricle  is  doing 

'  Deut.  Arch.  f.  klin.  Med.,  Ixxxiii,  1  and  2. 
=  Franke:   Wien.  klin.  Woch.,  1906,  No.  31. 


DISEASES    OF   THE    TRICUSPID    ORIFICE  95 

the  work  of  keeping  up  excess  pressure  in  tricuspid  insufficiency, 
just  as  the  right  ventricle  does  in  mitral  insufficiency.  ^  When  large 
quantities  of  blood  are  penned  up  in  the  veins  however,  the  left 
ventricle  has  less  to  handle  and  maj^  decrease  in  size.- 

In  children  the  tendency  to  tricuspid  insufficiency  is  minimized 
by  the  more  horizontal  position  of  the  heart.  Gravity  has  thus 
little  effect.  The  negative  pressure  created  by  ventricular  diastole, 
plus  the  auricular  systole,  are  the  chief  factors  in  filling  the  ven- 
tricle (Fetterolf  and  Gittings). 

Relative  tricuspid  insufficiency  is  a  common  lesion.  Structurally 
this  valve  is  inferior  to  the  mitral,  and  with  dilatation  of  the 
right  heart  incompetency^  is  readily  induced.  This  is  due  not 
onh'  to  relaxation  of  the  tricuspid  sphincter,  but  more  especially 
to  the  fact  that  in  dilated  hearts  the  origins  of  the  chordse  tendinese 
and  the  papillary  muscles  are  too  far  from  the  center  of  the  ven- 
tricular cavity  to  permit  perfect  valvular  closure.^  Tricuspid 
insufficiency  may  occur  during  parturition,  and  in  various  forms 
of  prolonged  and  arduous  labor  which  necessitate  great  muscular 
and  intrathoracic  straining. 

Clinical  Considerations. — Gibson  has  stated  that  tricuspid 
insuflficiency,  far  from  being  a  rare  lesion,  is  the  commonest  of 
all  valvular  insufficiencies.  This  is  probably  correct  if  we  include 
the  functional  regurgitation  which  occurs  after  the  manner  of  a 
safety-valve  under  great  muscular  strain,  and  under  other  condi- 
tions of  increased  right  ventricular  pressure.  The  sweeping  state- 
ment of  Romberg,  that  "isolated  tricuspid  insufficiency  has  not 
j^et  been  described,"  evidently  does  not  refer  to  the  relative 
insufficiency  above  referred  to.  The  safety-valve  effect  alluded 
to,  which  was  first  emphasized  by  T.  W.  King,  of  "moderator 
band  fame,"  although  it  had  been  described  b.y  earlier  writers,  is 
by  no  means  universally  accepted  as  a  fact. 

'  Calvert:  Arch.  Int.  Med.,  April,  1908. 

^Stadler:  Arch.  f.  klin.  Med.,  190.5,  Ixxxiii,  Heft  1  und  2. 

'  Krehl:  Arch,  f,  Anat.  u.  Physiol.,  1889,  p.  289. 


VI.  DISEASES  OF  THE  PULMONARY  ORIFICE 

"  Steucturally  the  pulmonary  valve  and  its  surroundings 
differ  from  those  of  the  aortic  valve  in  their  more  delicate  texture, 
and  in  the  fact  that  in  the  adult  the  segments  do  not,  as  a  rule, 
show  the  medial  thickening  about  the  corpora  Arantii.  The  wall 
of  the  pulmonary  artery  is  thinner  than  that  of  the  aorta  and  has 
not  the  same  tendency  to  preserve  its  ring  structure  in  the  absence 
of  an  internal  pressure.  The  conus  arteriosus  which  leads  into 
the  pulmonary  arterj^  is  more  thin-walled  than  the  corresponding 
part  of  the  left  ventricle,  and  under  increased  internal  pressure  is 
probably  capable  of  considerable  dilatation.  The  structures  in 
relation  to  the  pulmonary  valve  are  obviously  directed  as  a  whole 
to  withstanding  much  less  pressure  than  the  corresponding  parts 
of  the  aorta,  and  this  is  borne  out  by  what  is  known  regarding 
the  relative  pressures  in  the  two  sides  of  the  heart.  "^  Among 
4,547  autopsies  and  238  cases  of  valvular  disease  Willigk  found 
9  cases  of  pulmonar}^  endocarditis. 

PULMONARY  OBSTRUCTION 

Pathogenesis. — Obstruction  of  the  pulmonary  orifice  is  one  of 
the  most  rarely  acquired,  and  the  commonest  of  congenital,  val- 
vular lesions  of  the  heart.  It  maj'  be  produced  by  infectious  dis- 
eases, yet  often  no  such  history  is  obtainable.  Some  of  the  cases 
have  been  due  to  sclerotic  or  gummatous  syphilitic  lesions.  Again, 
pulmonarj^  stenosis  may  result  from  pressure  from  an  aortic 
aneurism  or  tumor.  Some  cases  have  been  ascribed  to  a  fetal 
endocarditis;  against  this  hypothesis  is  the  fact  that  the  inflam- 
matory condition  should  remain  so  localized.  In  one  case  re- 
ported by  Dittrich  the  etiologic  factor  appeared  to  be  the  kick  of 
a  horse  on  the  precordium.-     From  both  an  anatomic  and  an 

'  Osier  and  Gibson:   Osier's  "Modern  Medicine,"  vol.  iv,  p.  251. 
^  Dittrich:  Vierteljahrsch.  f.  prakt.  Heilkunde,  1849,  p.  1.57. 
96 


DISEASES    OF   THE    PULMONARY    ORIFICE  97 

etiologic  standpoint  obstruction  of  the  pulmonary  orifices  is 
divided  into  two  classes:  (a)  stenosis  the  result  of  acquired  patho- 
logic alterations;  (fe)  atresia,  the  result  of  congenital  malformation. 
Narrowing  may  occur  either  at  the  orifice  proper,  in  the  first 
part  of  the  artery,  or  in  the  conus  arteriosus.  Not  infrequently 
insufficiency  of  the  valve  also  exists. 

Morbid  Anatomy. — In  the  majority  of  cases  pulmonary  stenosis 
is  due  to  an  abnormalitj^  or  hypoplasia  of  some  part  of  the  pul- 
monary tract,  such  as  the  conus,  in  which  the  leaflets  themselves 
may  or  may  not  be  involved.  "In  these  cases  a  defect  of  the 
interventricular  septum  is  usually  associated  and  a  deviation  to 
the  right  of  the  aorta,  so  that  this  arises  from  both  ventricles 
above  the  defect.  Such  forms,  which  seem  to  suggest  a  develop- 
mental origin,  make  up  the  great  majority  of  cases  of  pulmonary 
stenosis,  and  the  combination  of  these  three  conditions,  pulmonary 
stenosis,  defect  of  the  septum  at  the  base,  and  rechtslage  of  the 
aorta,  is  probably  the  commonest  of  all  cardiac  anomalies" 
(Abbott).  Some  cases  result  from  induration,  thickening,  fusion, 
or  calcification  of  the  valve  leaflets  without  other  structural  defects, 
and  are  manifestly  the  result  of  an  inflammatory  process.  Ac- 
cording to  Keith,  the  conus  of  the  right  ventricle  is  involved  in 
90  per  cent,  of  the  cases.  In  most  of  the  cases  the  right  auricle 
and  ventricle  are  hypertrophied  and  dilated.  With  increasing 
stasis  tricuspid  insufficiency  is  often  superadded. 

Pulmonarj'  stenosis  seems  distinctly  to  predispose  to  tubercu- 
lous disease  of  the  lungs.  Among  449  cases  of  the  former  there 
were  160  of  the  latter.^ 

Pathologic  Physiology. — "In  congenital  cases  the  effect  on 
the  lioart  depends  largely  on  the  state  of  cardiac  development 
at  which  the  pulmonary  narrowing  is  produced.  If  it  appears 
before  the  end  of  the  third  month,  the  interventricular  septum 
does  not  close;  if  after  this  date,  the  foramen  ovale  and  ductus 
arteriosus  may  remain  patent.     The  condition  of  the  right  ven- 

'  (!.  W.  .Norris:   "Tiiljt-rculo.si.s  ami  iJcurt  Disoasc,"  Airi.  Jour.  Med.  Sci.,  Oct.,  li)0-l. 


98  STUDIES   IN    CARDIAC    PATHOLOGY 

tricle  varies  with  the  degree  of  occlusion  of  the  pulmonic  orifice. 
If  the  opening  is  completely  blocked,  the  ventricle  may  remain 
small  and  undeveloped,  but  with  less  degrees  of  narrowing  the 
chamber  is  commonly  greatly  hypertrophied "  (Colbeck). 

PULMONARY  INSUFFICIENCY 

Pulmonary  insufficiency  is  a  rare  lesion.  Only  one  case  was 
found  among  8,640  autopsies  at  the  Philadelphia  Hospital,  and 
24,000  medical  cases  admitted  to  the  Johns  Hopkins  Hospital 
revealed  only  3  cases. 

Pathogenesis. — Pulmonary  insufficiency  may  result  from  in- 
fective endocarditis,  or  from  the  long-continued  pulmonary  hyper- 
tension which  occurs  in  mitral  disease,  emphysema,  and  other 
forms  of  chronic  lung  disease.  Pitt  has  called  attention  to  its 
relative  frequency  as  a  result  of  gonorrheal  endocarditis.  It  occurs 
in  both  sexes,  is  a  disease  of  early  life,  and  is  usually  associated 
with  obstruction.  Sometimes  pulmonary  sclerosis  may  be  simply 
a  part  of  a  general  systemic  process.  Pulmonary  incompetence 
may  result  from  congenital  malformation,  although  as  a  rule  such 
abnormalities,  which  are  relatively  frequent  and  generally  consist 
either  of  an  increase  or  a  diminution  of  the  number  of  leaflets, 
are  unproductive  of  leakage.  Among  the  Philadelphia  Hospital 
autopsies  (8,640)  there  were  5  cases  of  supernumerary  leaflets, 
other  anomalies  4,  fenestration  17.  (See  Fig.  81.)  At  times 
pulmonary  incompetence  results  from  aneurism  or  rupture  of  a 
valve. 

From  a  study  of  172  reported  cases  of  sclerosis  of  the  pulmonary  artery 
Posselt  found  the  following  conditions  associated:  mitral  stenosis,  47;  myo- 
carditis, 25;  arteriosclerosis,  21;  polyarthritis,  20;  aneurism  of  the  pulmonary 
artery,  18;  other  cardiac  lesions,  17;  patulous  ductus  Botalli,  15;  adhesive 
pericarditis,  15;   syphihs,  12;  emphysema,  12,  etc' 

It  is  probable  that  a  relative  insufficiency  due  to  dilatation 
also  occurs  when  pressure  in  the  pulmonary  circuit  is  much  in- 
creased.    Gibson  has  shown  that  in  a  normal  human  heart  post 

'  Lubarsch  and  Ostertag's  Ergebnisse  d.  allg.  Path.,  1909,  i,  444. 


DISEASES    OF   THE    PULMONARY    ORIFICE  99 

mortem   the  pulmonary  valve  begins  to  leak  when  pressure   is 
raised  to  from  16  to  26  c.c.  of  mercury. 

Pathologic  Anatomy. — Well-marked  changes  in  the  endocardium 
of  the  right  heart  in  cases  of  pulmonary  insufficiency  are  not 
often  found.  The  pathologic  alterations  which  are  frequently 
encountered  in  the  left  heart  when  the  valves  are  incompetent 
are  generally  absent  or  but  slightly  marked.  The  pulmonary 
leaflets  are  less  thickened  and  atrophy  or  sclerosis  of  the  endo- 
cardium is  less  markedly  evident.  There  is,  however,  generally 
a  dilatation  of  the  right  ventricle  and  of  the  conus  arteriosus.^ 

An  unusual  case  of  pulmonary  endocarditis  causing  perforation  of  the  ven- 
tricular septum  followed  by  embolic  gangrene  of  the  nose  and  ears,  and  multiple 
infarcts  in  the  kidneys,  has  been  reported  by  Fisher  and  Longcope.-  Reitmann ' 
has  reported  symptomless  pea-sized  hyalo-fibromas  in  the  nodules  of  Arantius 
of  the  anterior  pulmonary  leaflet  in  a  patient  of  seventy-four  years. 

Isolated  atheroma  and  dilatation  of  the  pulmonary  artery  has  been  generally 
regarded  as  of  considerable  variety.  Romberg's  case  has  been  extensively 
quoted  in  the  literature,  and  a  few  other  cases  are  on  record.  L.  Rogers  has 
recently  reported  10  cases,  and  states  that  the  condition  is  not  infrequent  in 
Bengal,  where  his  material  was  collected. 

Marked  hypertrophy  of  the  right  ventricle  was  observed,  the  patients  dying 
with  symptoms  of  right  heart  failure,  and  frequently  showing  hydropericardium, 
resulting  from  dilatation  of  the  coronary  veins.  The  valve  leaflets  nearly  always 
escaped.  Contrary  to  other  forms  of  arteriosclerosis,  it  occurred  most  frequently 
in  women.  The  explanation  seems  to  lie  in  the  fact  that  these  cases  are  syphilitic 
in  origin.  Disease  of  the  pulmonary  artery  has  also  been  attributed  to  the  arti- 
ficial plethora  of  prolonged  and  excessive  beer-drinking.'*  While  doubtless  most 
cases  of  sclerosis  of  the  pulmonary  artery  are  secondary  to  such  cardiac  lesions 
as  lead  to  tricuspid  insufficiency,  yet  some  cases  have  been  reported  in  which  the 
pulmonary  sclerosis  seemed  to  be  the  primary  lesion.^  The  most  important 
factors  are  mechanical — increased  or  variable  blood-pressure,  in  which  intoxica- 
tion and  infection  perhaps  also  play  a  role." 

'  Zahn:  Vcrhandl.  d.  Konsr.  f.  inn.  Med.,  190.5,  p.  359. 

^  Fi.sher  and  Longcope:  Proc.  Path.  Soc.  Phila.,  1903,  p.  98. 

'  Reitmann:  Zeit.  f.  Heilk.,  xxvi,  Abth.  f.  path.  Anat.,  Heft.  I. 

*  Kitamura:  Zeit.  f.  khn.  Med.,  Ixv,  Heft.  I  and  II. 

•'■  Sanders:  Arch.  Internal  Medicine,  April,  1909. 

'  Laubry  and  Parvu:  Tribune  Med.,  1909,  p.  485. 


VII.  ACUTE  PERICARDITIS 

Occurrence.^ — Pericarditis  may  occur  in  any  form  of  general 
infection.  Brooks  and  Lippincott^  found  that  46  out  of  67  cases 
were  due  to  general  bacterial  infections.  Some  of  these  diseases, 
such  as  rheumatic  fever  and  pneumonia,  however,  are  much  more 
prone  than  others  to  be  thus  complicated.  It  is  apparently  more 
common  in  children  than  in  adults,  especially  in  the  rheumatic 
fever  of  the  second  decade,  and,  as  might  be  expected,  in  chorea 
(19  out  of  73  autopsies — Osier).  Andrew  among  1,474  cases  of 
heart  disease  found  25  cases  of  pericarditis. 

Pathologic  Anatomy. — The  earliest  manifestation  of  pericarditis 
consists  in  a  vascular  engorgement,  which  spreads  from  the  course 
of  the  larger  vessels  as  the  process  advances.  Small  localized 
granulomas  occur  chiefly  at  the  base  of  the  heart.  Associated 
with  this  vascular  injection  the  normally  transparent  and  glistening 
membrane  becomes  cloud}'  and  roughened  as  the  result  of  fibrous 
exudation  and  of  tumefaction  of  the  endothelium.  If  the  deposi- 
tion of  fibrin  increases,  it  is  formed  into  ridges  by  the  friction  of 
cardiac  contraction,  producing  a  reticulated  appearance  which 
has  been  compared  to  honeycomb,  the  rippled  sea,  the  rugse  of 
the  second  stomach  of  the  calf  (Corvisart),  buttered  bread,  two 
slices  of  which  have  been  separated  (Laennec). 

Following  the  inflammatory  engorgement  there  may  be  more 

'Brooks  and  Lippincott:  Am.  Jour.  Med.  Sci.,  Dec,  1909. 


Fig.  29. — Fibhinopurulent  Pericarditis. 

D.  AI.,  male,  aged  thirty-six  years.  (Philadelphia  Hospital,  vol.  xvii,  p.  141.  Physician: 
Dr.  Hawke.     Pathologist:  Dr.  A.  J.  Smith.) 

P.\THOLOGic  Diagnosis:  Croupous  pneumonia  of  right  upper  lobe,  plastic  pleuritis, 
fibrinopurulent  pericarditis,  etc. 

Autopsy  Notes:  The  pericardium  contains  300  c.c.  of  slightly  brownish,  thin,  turbid 
fluid.  Both  the  visceral  and  parietal  layers  are  covered  with  a  layer  of  yellowish  plastic  exudate, 
mth  the  characteristic  villosities  and  lines.  The  heart  with  its  contained  blood  and  with  the  peri- 
cardium weighs  880  gm.     Circumference  at  the  base  78  cm.     External  length  of  ventricle,  1 1  cm. 


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102  STUDIES    IN    CARDIAC    PATHOLOGY 

or  less  liquid  exudation,  which  may  be  simply  serous  or  a  mixture 
of  serum  with  fibrin,  blood,  or  pus.  In  rheumatic  fever  the  exudate 
is  generally  serofibrinous.  Purulent  cases  are  particularly  frequent 
in  childhood,  and  when  the  pneumococcus  is  the  offending  organism. 
Blood-stained  exudates  are  met  with  in  tuberculous,  cancerous, 
purpuric,  scorbutic  cases,  and  in  the  terminal  stages  of  Bright's 
disease.  At  times  considerable  blood  may  be  found  without 
evident  cause;  such  cases  probably  result  from  microscopic  vas- 
cular lesions. 

A  simple  serous  effusion  may  be  absorbed  without  permanent 
damage.  If  fibrin  is  present,  adhesions  are  apt  to  form  when  the 
parietal  and  visceral  layers  again  come  in  contact.  Sometimes 
such  adhesions  may  be  broken  up,  or.  again,  permanent  synechiae 
may  remain.  The  distinction  between  fibrinous  and  serofibrinous 
pericarditis  is  one  of  degree  only;  the  essential  process  is  the  same. 
According  to  Ziegler,  vascularization  of  the  exudate  from  the 
vessels  on  the  pericardial  surface  begins  by  the  third  or  fourth 
day.  Under  favorable  circumstances  more  or  less  complete 
resorption  of  even  a  fibrinous  exudate  may  occur,  only  a  small 
circumscribed  macula  or  adhesion  remaining.  As  a  rule,  the 
visceral  layer  shows  the  most  marked  changes  on  account  of  its 

Fig.  30. — Subacute  Fibrinous  Pericarditis. 

,J.  M.,  male,  aged  thirty  years.  (Pennsylvania  Hospital.  Autopsy  1.57.  Phj-sician: 
Dr.  Stengel.     Pathologist:  Dr.  Longcope.) 

Clinical  Notes:  Never  ill  until  two  months  ago,  when  he  developed  pain  in  the  left  side 
of  the  thorax.  This  eventually  proved  to  be  an  empyema,  which  was  opened  and  drained  at 
the  hospital  (Dr.  Spellissy).  Heart  dullness  was  increased  laterally.  The  apex-beat  was 
neither  palpable  nor  visible.     Death  occurred  gradually. 

Pathologic  Diagnosis:  Subacute  fibrinous  pericarditis.  Fibroid  tuberculosis;  bronchi- 
ectasis, etc. 

The  left  lung  is  densely  adherent  to  the  pericardium  along  its  entire  length,  both  lungs 
being  adherent  to  the  parietal  pleura,  just  below  the  opening  of  a  small  sinus  which  leads  from 
the  abscess  cavity. 

The  pericardium  is  adherent  to  epicardium,  and  its  sac  contains  a  small  amount  of  purulent 
fluid.  Between  the  pericardium  and  epicardium  there  is  a  thick  fibrinous  network  of  adhesions, 
giving  it  a  "bread  and  butter"  appearance.  The  heart  muscle  is  soft  and  moderately  pale. 
The  epieardial  fat  is  abundant,  and  strands  of  connective  tissue  can  be  seen  running  into 
the  heart  muscle.  The  left  ventricle  measures  2  cm.  in  thickness.  The  valves  are  normal; 
pulmonic  orifice  S..5  cm.,  aortic  8  cm.,  in  circumference. 


104  STUDIES  IN  CARDIAC  PATHOLOGY 

greater  vascularity  and  activity.  When  pyogenic  organisms  are 
present,  a  great  outpouring  of  leukocytes  occurs;  the  liemorrhagic 
form  is  merely  the  result  of  the  addition  of  erythrocj^es.  Trauma 
may  play  both  a  direct  and  an  indirect  role  in  the  production  of 
pericarditis.  Puncture,  the  injection  of  turpentine,  blows  upon 
the  precordium,  mediastinal  irritation  due  to  prolonged  passage 
of  a  stomach-tube,  may  produce  pericarditis.  The  scant  blood- 
supply  of  the  sac  doubtless  favors  infection,  and  the  toxin  developed 
in  its  neighborhood  seems  to  have  a  predisposing  effect  (Charrin). 
The  experimental  work  of  Kuelbs  showed  that  when  pericardial 
lesions  resulted  from  precordial  blows,  they  were  generalh'  slight 
and  consisted  of  small  hemorrhages. 

The  serofibrinous  form  occurs  very  frequently  in  pneumonia, 
infection  seeming  to  take  place  through  the  pleura  or  mediastinum. 
The  auricles  are  first  and  chiefly  involved,  the  visceral  layer  show- 
ing changes  later.  As  the  disease  advances  small  inflammatory 
areas  coalesce  until  the  whole  heart  may  be  enveloped  in  a  thick, 
yellowish,  fibrinous  mold. 

The  chemical  constituents  of  an  inflammatory  pericardial  exudate 
are  practically  those  of  the  normal  secretion.  In  some  cases, 
especially  the  nephritic  ones,  both  alcohol-  and  water-soluble 
extractives  are  somewhat  increased  (Erben).^ 

A  normal  pericardium  has  a  capacity  of  from  180  to  200  c.c. 
As  large  an  amount  as  800  c.c.  can  be  forced  into  the  sac,  but 
anything  beyond  this  is  due  to  stretching — actual  enlargement 
of  the  membrane  (Schaposchikoff  and  Damsch).  The  effusion  of 
disease  is  often  much  larger  than  could  be  forced  into  a  normal 
pericardium.  As  was  pointed  out  by  Smith  and  Lusk,  this  is 
accounted  for  by  a  softening  and  stretching  of  the  sac  which 
results  from  the  inflammatory  processes.  The  fact  that  exudates 
are  not  absorbed  from  an  inflamed  pericardium  as  they  are  if 
drained  into  a  healthy  serous  cavity,  as,  for  example,  the  pleura, 

'  Erbcn :  Klin.  u.  Cheni.  Beitrage  z.  Lehre  der  exud.  Pericarditis,  Vienna,  1905. 


ACUTE    PERICARDITIS  105 

is  perhaps  due  to  pressure  of  the  exudate  upon  the  stomas,  and 
upon  the  fact  that  these  are  plugged  with  fibrin.^ 

Purulent  pericarditis  arises  if  pj^ogenic  organisms  are  introduced 
either  by  way  of  the  blood-stream  or  the  lymphatics,  or  by  direct 
rupture  of  an  abscess  into  the  sac.  Two  instances  of  the  latter 
cases  occurred  among  my  8,640  autopsies.  When  a  serofibrinous 
exudate  undergoes  transition  into  a  purulent  one,  the  fibrin  becomes 
more  or  less  liquefied.  As  a  rule,  suppurative  exudates  are  smaller 
than  serofibrinous  ones.  Gas  is  sometimes  found  in  the  sac, 
produced  by  the  bacillus  aerogenes  capsulatus.  Some  j^ears  ago 
James-  collected  38  cases  of  pneumopericardium.  Twenty-six 
were  fatal.  Among  those  which  recovered,  4  were  due  to  stab 
wounds  and  4  to  other  forms  of  trauma. 

Penetrating  wounds  generally  produce  the  purulent  form  of 
the  disease.  Rareh'  such  perforation  may  occur  from  some  object 
lodged  in  the  esophagus.  Flint  reported  such  a  case  in  which 
the  offending  object  was  a  set  of  false  teeth.  Some  very  large 
liquid  exudates  have  from  time  to  time  been  reported:  Sir  A. 
Clark,  4  liters  of  seropurulent  effusion;  Osier,  2  to  3  liters;  Hirtz, 
2,790  c.c;    Thayer,  4,000  c.c. 

The  different  varieties  of  pericarditis  have  been  reported  with 
the  following  freciuency: 

BreITUNG.  NORRIS.  NORRIS. 

(Charite,  (Philadelphia  (Pennsylvania 

Berlin.)  Hospital.)  Hospital.) 

Sero-fibrinous 108  132  44 

Purulent 24  23  39 

Hemorrhagic 30  18  3 

Tuberculou.s 2(5  (2  primary?)    22  9 

Chronic  fibrous Ill  .304  24 

Obliterative 23  16  6 

Calcification 2  7  1 

Total  number  of  cases .324  .529  126 

Among  120  cases  of  ])ericarditis  at  th(!  Pennsylvania  Hos})ital 

'  JJerginann  (Charitd  Annalen,  1909,  p.  92) ;  A  case  of  large  pericardial  effusion  was  tapped 
.so  that  it  emptied  itself  into  the  healthy  pleura,  whence  it  was  rapitlly  and  spontaneously 
absorbed  within  throe  days. 

^.James:  American  Medicine,  .July  2,  1904. 


106  STUDIES  IN  CARDIAC  PATHOLOGY 

cultures  were  made  from  the  exudate  in  54  cases,  with  the  following 
bacteriologic  findings: 

Micrococcus  lanceolatus 14 

Pneumococous 10 

Sterile 10 

Unidentified  species 6 

Streptococcus  pyogenes 5 

Bacillus  coli  communis 3 

Bacillus  lactis  aerogenes , 2 

Bacillus  proteus  vulgaris 1 

Micrococcus  zymogenes 1 

Mixed  infections  (included  above) 4 

Tubercle  bacillus 1 

Streptococcus  mucosus 1 

Contaminated  cultures 2 

The  following  pathologic  conditions  were  associated  with 
pericarditis:  Lobar  pneumonia,  43;  bronchopneumonia,  9;  acute 
endocarditis,  20;  chronic  endocarditis,  28;  tuberculosis,  18; 
empj^ema,  11;    mediastinitis,  3;    typhoid  fever,  4. 

Previous  disease  or  trauma  may  prepare  the  soil  for  subsequent 
pericardial  infection.  Such  infection  may  occur  by  way  of  the 
blood-stream,  the  lymphatics,  hj  direct  extension,  or  by  perfora- 
tion. 

The  parietal  layer  of  the  pericardium,  according  to  Bizzozero  and  Salvioli,^ 
contains  a  single  network  of  lymphatics,  which  lie  deeply  embedded  in  the  con- 
nective-tissue stroma,  and  consist  of  interlacing  vessels.    Schwartzoff  -  has  shown 

'  Bizzozero  and  Salvioli:   Arch,  delle  Scienze  Mediche,  vol.  ii. 

^  Schwartzoff:  Materialen  z.  Anat.  u.  Histol.  d.  Herzens  u.  s.  Huellen,  1874 


Fig.  31. — Fibrinous  Pericarditis. 

G.  B.,  laborer,  negro;  aged  twenty-six  years.  (Pennsylvania  Hospital,  November  16, 
1909.     No.  2763.     Autopsy:  9.34.     Pathologist:   Dr.  Crispin  ) 

Anatomic  Diagnosis:  Lobar  pneumonia  of  whole  right  lung.  Fibrinous  pericarditis 
with  effusion.  Fibrinous  pleuritisof  right  side,  etc.  Cloudy  swelling  of  heart,  liver,  kidneys, 
etc. 

Heart:  Is  of  usual  size,  weighs  330  gm.  It  is  covered  with  a  thick,  boggy,  shaggy,  yellow, 
fibrinous  exudate.  The  pericardial  cavity  contains  600  c.o.  of  yellow  fluid,  turbid  with  fibrin- 
ous shreds  and  flecks.  The  right  auricle  is  of  normal  size,  its  tips  free  from  thrombi.  Tri- 
cuspid normal;  also  the  pulmonary.  The  anterior  leaflet  of  the  mitral  valve  has  quite  a  thick 
fibrous  edge,  but  the  chordos  are  not  much  thickened  or  shortened.  Papillary  muscles  are  pale  and 
thickened.  Ventricular  wall  IS  to  SO  mm.  and  very  cloudy.  There  are  a  few  yellow  plaques  on 
the  arterial  wall  about  the  aortic  valves. 

Microscopic  Examination:  The  exudate  covering  the  pericardium  contains  a  moderate 
number  of  polynuclear  cells.  The  muscle-cells  are  much  swollen  and  have  a  waxy  appearance 
(parenchymatous  degeneration). 

Bacteriologic  Examination:  From  both  lungs  and  from  the  pericardial  exudate  small 
cocci  were  obtained,  occurring  in  pairs,  and  Gram-positive. 


108  STUDIES    IN    CARDIAC    PATHOLOGY 

that  these  vessels  drain  into  the  glands  which  lie  in  the  areolar  tissue  between  the 
pleura  and  pericardium.  The  lymphatics  in  the  visceral  layer  are  much  richer 
and  intercommunicate.  Nystrom '  considers  the  question  debatable  as  to  whether 
the  lymphatics  of  the  pericardial  cavity  communicate  with  those  of  the  external 
layer.  It  would  have  to  be  assumed,  therefore,  that  when  the  pericardium  is 
infected  from  the  bronchial  glands  the  micro-organisms  travel  in  a  direction 
opposite  to  the  lymphatic  current,  as  may  occur  in  carcinoma  metastases. 

Pathogenesis. — Pericarditis  occurs  chietij"  in  infectious  dis- 
eases— rheumatic  fever,  pneumococcic,  gonococcic,  streptococcic 
septicemias,  also  in  tuberculosis,  syphilis,  and  scarlatina.  It 
occurs  as  a  terminal  infection  in  dyscrasic  states,  such  as  chronic 
nephritis,  diabetes,  leukemia,  etc.  More  rarely  it  follows  from 
the  direct  extension  of  an  empyema,  a  subdiaphragmatic,  medias- 
tinal abscess,  or  from  penetrating  wounds  or  the  infiltration  of 
neoplasms.  Frequently  pericarditis  and  endocarditis  are  asso- 
ciated. In  rheumatic  fever,  for  instance,  this  is  common.  In  the 
suppurative  pericarditis  of  childhood,  however,  which  is  nearly 
always  secondary  to  pulmonar}^  disease,  the  endocardium  gen- 
erall}^  escapes.  Sixty  per  cent,  of  the  pericarditis  of  childhood 
results  from  empyema,  the  rest  being  made  up  by  abscesses, 
osteom3'elitis,  pyemia,  etc- 

At  the  Philadelphia  Hospital  among  75  cases  of  acute  aortic 
endocarditis  there  were  20  cases  of  pericarditis;    among  75  cases 

'  Nystrom:   Arch.  f.  anat.  u.  Physiol.  Anat.,  Abth..  1S97,  p.  361. 
-  Poynton:  Heart  Disease  and  Thoracic  Aneurism,  1907,  p.  168. 

Fig.  32. — Adhesive  Pericarditis — Cor  Villosum. 

Wm.  M.,  male,  aged  fifty-six  years.  (Philadelphia  Hospital,  vol.  xvii,  p.  217.  Physician: 
Dr.  Musser.     Pathologist:  Dr.  Coca.) 

Pathologic  Diagnosis:  Chronic  parenchymatous  and  interstitial  nephritis,  with  renal 
infarction.     Adhesive  pericardilis — cor  villosum — acute  valvulitis,  etc. 

Clinical  History:  The  patient,  a  moderate  consumer  of  alcohol,  was  admitted  complain- 
ing of  dyspnea,  cough,  and  asthenia,  the  first-named  having  been  present  for  a  number  of 
years.     Temperature  101°,  pulse  SO,  respiration  30,  on  admission. 

Physical  Examination:  The  apex-beat  was  not  palpable.  The  heart -sounds  were  al- 
most entirely  obscured  by  rales.  The  pulse  was  weak  and  irregular.  The  heart-sounds  at  the 
base  were  inaudible  and  this  organ  was  enlarged  to  percussion.  A  sudden  convulsion  was 
followed  by  unconsciousness,  ending  in  death  from  edema  of  the  lungs.  Exploratory  puncture 
of  the  pericardium  had  given  negative  results. 


110  STUDIES  IN  CARDIAC  PATHOLOGY 

of  acute  mitral  endocarditis  there  were  18  cases  of  pericarditis; 
among  10  cases  of  acute  tricuspid  endocarditis  there  were  5  cases 
of  pericarditis. 

Among  the  other  lesions  found  there  were  fatty  infiltration 
of  the  pericardium  99,  hydropericardium  199,  pigmentation  1, 
maculae  albidse  (exclusive  of  chronic  pericarditis),  84.  Brooks 
and  Lippincott  found  pleural  lesions  in  136  of  150  cases,  acute 
endocarditis  in  10  out  of  46,  chronic  endocarditis  in  28  out  of  67, 
acute  mj^ocarditis  in  2  out  of  67. 

Hemopericardium  results  from  rupture  of  a  blood-vessel  into 
the  sac.  Such  vessels  ma}'  be  the  aorta,  the  coronary  arteries 
or  veins,  superficial  vessels  injured  during  aspiration,  or  new 
vessels  formed  in  the  course  of  inflammatory  changes.  In  the 
latter  case  the  blood  is  generall}^  mixed  with  the  exudate.  At  the 
Philadelphia  Hospital  there  were  16  cases  of  hemopericardium 
in  8,640  autopsies.  In  cases  in  which  death  has  resulted  from 
asphj^xia,  small  subpericardial  ecchymoses  are  sometimes  found, 
especially  at  the  base  in  the  neighborhood  of  the  epicardial  vessels 
— "spots  of  Tardieu."     (See  Figs.  40  and  41.) 

Anthracosis  of  the  pericardium  has  been  reported  by  Askanazy.^ 

From  a  clinical  standpoint  rheumatic  fever  is  generallj^  stated 
to  be  the  most  common  cause  of  pericarditis.  Among  1,000 
cases  of  this  disease  at  the  Bethanien  Hospital  in  Berlin,  peri- 
carditis occurred  in  100,  and  endocarditis  in  250  of  the  cases. 
Well-marked  effusion  was  present  in  35  per  cent,  and  slight  effusion 
in  14  per  cent,  of  these;    aspiration  was  necessarj'  in  16  cases. - 

Rheumatic  fever  has  been  credited  as  the  causative  factor  of  pericarditis,  as 
follows:  Von  Schroetter,  30  per  cent.;  Harras,  7  per  cent.;  McCrae,  5.9  per 
cent.;  Williams,  75  per  cent.;  Leudet,  22  per  cent.;  Bamberger,  30  per  cent.; 
Bauer,  16  to  20  per  cent. ;  Chambers  and  Thompson,  20  to  30  per  cent. ;  Phillipps, 
4.7  per  cent.;  Ball  and  Sibson,  20  per  cent.;  WunderHch,  19  per  cent.;  Duchek, 
16  per  cent.;  Latham,  5  per  cent. ;  Telter,  4.7  per  cent.;  Eichhorst,  3  per  cent. ; 
Taylor,  50  per  cent. ;    Poynton,  75  per  cent,  (fatal  cases) ;   Dunn,  19  per  cent. 

'  Askanazy:  Zcntralb.  f.  path.  Anat.,  1906,  No.  16,  17. 
-  Zinn:  Therap.  d.  Gegenwart,  September,  1909. 


I'lc.  '4'-j. — Chronic  Adhesive  Pericarditis. 

Showing  almost  complete  obliteration  of  the  sac,  with  marked  thickening  and  extensive 
extrapericardial  adhesions.     (Specimen  from  the  German  Hospital.) 


112  STUDIES  IN  CARDIAC  PATHOLOGY 

(children) ;  Flint,  38  per  cent. ;  Ormerocl,  37  per  cent.  We  must  bear  in  mind, 
however,  that  "rheumatism"  is,  and  to  an  even  greater  extent  was,  a  much 
abused  disease;  many  different  forms  of  sepsis  being  included  in  the  term.  In 
Sears'  100  cases  of  rheumatism,  pericarditis  occurred  in  51  per  cent.  The  fre- 
quency of  rheumatic  infection  as  an  etiologic  factor  has  also  been  corroborated 
by  the  experimental  investigations  of  Wassermann,  Poynton  and  Paine,  Cole, 
Walker  and  others.  Sturges  in  100  fatal  cases  of  heart  disease,  of  which  54  were 
of  rheumatic  origin,  found  pericarditis  in  all  but  6.  Although  there  are  many 
exceptions,  the  pericarchtis  of  rheumatic  fever  generally  occurs  relatively  early 
in  the  attack — within  the  first  two  weeks.  Chronic  valvular  lesions  with  hyper- 
trophy, dilatation,  and  overaction  undoubtedly  predispose  to  it. 

As  long  ago  as  1600,  Guarinon  called  attention  to  the  frequency 
of  pneumonia  as  a  causative  factor  of  pericarditis;  in  fact,  this 
infection  was  blamed  for  the  majority  of  cases  until  Bouillaud 
emphasized  the  importance  of  rheumatic  fever.  Acute  pericarditis, 
either  serous,  plastic,  or  purulent,  occurred  289  times  among  2,439 
pneumonia  autopsies  (11.8  per  cent.),  and  499  times  among 
40,773  cases  of  pneum^onia  (1.2  per  cent.)  collected  by  the  author. 
It  is  bjf  far  the  commonest  cardiac  complication,  therefore,  and 
stands  high  up  among  complications  in  general.  The  wide  varia- 
tion in  the  frequency  with  which  the  condition  has  been  reported 
by  different  observers  shows  that,  even  allowing  for  errors,  the 
condition  is  more  frequent  at  certain  times.  ^  That  pericarditis  is 
frequently  found  unexpectedl.y  at  autopsy  is  well  known. 

Infection  may  occur  through  the  blood-  or  the  lymph-streams,  but  quite 
often  results  from  direct  extension  from  infected  areas  of  the  lungs  and  pleurae. 
In  a  large  proportion  of  Jiirgensen's  cases  the  hngual  process  of  the  left  upper 
lobe  was  cHseased.  Sears  and  Larrabee  found  the  right  lung  diseased  in  10  out  of 
18  cases.  Chatard  noted  the  right  lung  in  13,  the  left  in  5,  and  both  lungs  in  13. 
Kerr  found  the  left  lower  lobe  involved  in  12,  the  right  lower  in  9,  the  right  middle 
in  2,  and  both  lower  in  3  cases.  J.  A.  Scott,  in  76  autopsies  on  lobar  pneumonia 
at  the  Pennsylvania  Hospital,  Philadelphia,  found  pericarditis  in  38  (50  per  cent.). 
In  20  (52.56  per  cent.)  the  exudate  was  serofibrinous,  in  17  (44.7  per  cent.)  puru- 
lent, and  in  one  case  the  pericardium  was  obliterated  by  chronic  inflammation. 
Among  40  cases  of  pericarditis  22  occurred  in  pneumonia ;  in  all  of  these  pleuritis 
coexisted,  and  in  6  cases  both  the  pericarditis  and  the  pl(?uritis  were  fibrinopuru- 
lent.     In  170  autopsies  in  pneumonia.  Lance  and  Kanthack  found  pericarditis 

1  Netter  found  pericarditis  in  pneumonia  during  the  years  1837,  1876,  1882,  1886,  and 
1890  much  more  frequently  than  in  the  intermediate  years. 


ACUTE    PERICARDITIS  113 

37  times.  It  was  associated  with  the  following  conditions:  acute  endocarditis, 
4;  pleuritis  or  empyema,  8;  peritonitis,  1;  meningitis,  1;  synovitis,  1;  pleuritis 
and  peritonitis,  2 ;  meningitis  and  peritonitis,  1 ;  pleuritis  and  endocarditis,  1 . 
Chatard  found  the  pneumococcus  in  the  pericardium  in  19  out  of  29  cases,  no 
other  important  organisms  being  cultivated. 

Some  j^ears  ago  the  writer  collected  from  various  hospitals  in 
Philadelphia  accurate  data  regarding  1,780  autopsies  performed 
on  the  subjects  of  tuberculous  disease,  and  found  82  cases  of 
tuberculous  pericarditis.'^  Among  these  statistics  cases  of  simple 
macular  albidse  were  omitted,  as  were  also  all  cases  in  which  there 
was  a  reasonable  possibility  that  the  pericarditis  may  have  been 
due  to  other  causes  than  tuberculosis. 

Actual  tubercles  were  found  in  32,  and  of  the  remaining  49,  a  careful  study 
of  the  records  failed  to  disclose  the  evidence  of  an  etiology  other  than  tuberculosis. 
While  there  were  in  the  majority  of  instances  no  data  as  to  the  microscopic  ap- 
pearance of  the  tissues,  it  seems  reasonable,  to  credit  the  existence  of  these  lesions 
to  a  tuberculous  process;  for  it  is  well  known  that  the  majority  of  pleural  scars 
and  adhesions,  so  frequently  found  at  autopsies,  arise  in  this  manner,  although 
even  the  microscope  fails  to  reveal  either  the  tubercle  bacillus  or  its  characteristic 
changes.  Jaccoud,^  in  1893,  reported  a  case  of  complete  pericardial  symphysis 
in  which  all  other  causes  could  be  positively  excluded,  and  in  which  tubercle 
bacilli  containing  mechastinal  glands  were  the  only  other  pathologic  lesions  found. 
In  1885  the  same  author  recorded  a  case  in  which  the  pericardium  was  macro- 
scopically  normal,  but  in  which  tubercle  bacilli  were  microscopically  demon- 
strable. In  Wells'  ^  24  cases  of  obliterative  pericarditis  the  bronchial  glands  were 
caseous  in  10  instances. 

In  tuberculous  pericarchtis  the  heart  muscle  at  times  undergoes  caseous 
infiltration  and  degeneration.  This  occurred  in  5  of  my  82  cases;  other  forms 
of  myocarditis,  fatty  or  fibroid  change,  are  more  common.  In  one  of  Osier's 
cases  a  thin  film  of  auricular  appendix  alone  was  found  intact ;  the  remainder  of 
the  cardiac  muscle  in  that  region  having  undergone  caseous  necrosis.  In  the 
chronic  varieties  of  this  disease  the  heart  is  frequently  enlarged;  at  first  hyper- 
trophied  by  an  effort  to  overcome  the  abnormal  resistance  caused  by  synechise, 
effusion,  or  constriction  of  the  large  vessels;  later,  dilated  through  overwork, 
malnutrition,  and  degeneration  of  its  muscle-fibers.  The  site  of  the  hyper- 
trophy, of  course,  dopenrls  on  the  location  of  the  increased  resistance.  The 
(|uestion  as  to  whethtT  liypcrtropliy  will  or  will  not  occur  depends  largely  on  the 

'  G.  W.  Norris:  Univ.  of  Pennsylvania  Med.  Bull.,  .luly,  1!)()1. 
^  .Jacfoucl :  Semainc  M(jdif;ale,  vol.  xiii,  ISOo,  p.  '21. 
•■•  \\i-\\<:  .(.iiir.  Am.  .Med.  Assoc,  May  25,  lOOI. 


114  STUDIES   IN    CARDIAC    PATHOLOGY 

integrity  of  the  blood-supply  and  the  state  of  the  myocardium  at  the  time  when 
the  adhesions  form. 

Tuberculous  pericarditis  may  occur  as  miliary  tubercles,  as  large  caseous 
masses,  or  as  simple  fibrous  thickening,  with  or  without  adhesions,  in  which 
microscopically  no  specific  tuberculous  changes  may  be  demonstrable.  With 
mixed  infections  any  variety  of  exudate  may  be  formed. 

The  effusion  in  tuberculous  pericarditis  may  consist:  (1)  Of  clear  serum,  its 
nature  being  only  demonstrable  through  the  presence  of  pericardial  tubercles  or 
tubercle  bacilli.  (2)  Turbid  or  flocculent  fluid  is  sometimes  encountered; 
usually  if  fibrin  is  present,  it  is  adherent  to  the  serous  membrane.  I  found  this 
condition  17  times.  (3)  Hemorrhagic  effusion  occurred  only  4  times,  once  coin- 
cidently  with  uremia.  Some  authors  have  stated  that  the  aspiration  of  sanguin- 
eous pericarcUal  fluid  should  lead  one  to  suspect  a  tuberculous  origin,  a 
statement  which  must  be  accepted  with  reservation.  (4)  Fibrinopurulent 
exudate  was  encountered  7  times.  In  none  of  these  cases  was  the  condition 
caused  by  the  rupture  into  the  pericarchum  of  a  tuberculous  lymph-node,  as 
happened  in  the  cases  reported  by  Zenker,'  Kast,-  Mickle,^  Heineman,''  and  Finzi.' 
The  amount  of  effusion  in  tuberculous  pericarditis  is  sometimes  enormous. 
The  largest  recorded  in  my  series  was  Musser's"  well-known  case,  in  which  1,559 
c.c.  of  hemorrhagic  fluid  was  removed  at  autopsy. 

The  varieties  of  pericarditis  as  occurring  in  my  series  of  tuberculous  peri- 
carditis may  be  tabulated  as  follows : 

1.  CHRONIC  FIBROPLASTIC. 

(a)  Complete  obliterative 24 

(b)  Partial  obliterative 19 

(c)  Non-obliterative 3 

2.  ACUTE  VARIETIES. 

(ti)  Serofibrinous 12 

(6)  Fibrinopurulent 7 

(c)  Fibrinoplastic .' 3 

(d)  Hemorrhagic 4 

(e)  Miliary 10 

Tuberculous  pericarchtis  has  been  found  more  commonly  in  men;  in  the 
present  series  it  was  overwhelmingly  so — 86  males,  11  females — the  sex  of  4  hav- 
ing been  unrecorded.  The  ages  ranged  from  seven  weeks  to  seventy-seven 
years,  showing  that  no  age  is  exempt.  The  former  is,  I  think,  the  earliest  time 
of  life  at  which  a  case  has  been  reported;  22  cases  occurred  in  negroes,  being 
probably  about  the  same  proportion  to  the  entire  series  as  the  percentage  of 
negroes  admitted  to  the  hospitals. 

'  Zenker:  Quoted  by  Osier,  Am.  Jour.  Med.  Sci.,  1S93. 

^  Kast:  Virohow's  Archiv.,  Bd.  xcvi. 

'  Mickle:   Lancet,  1883. 

'  Heineman:   Lancet,  Dec.  28,  1901. 

^  Finzi:   La  Riforma  medica,  Sept.  16,  1903. 

"  Musser:   University  Medical  Magazine,  Oct.,  1888,  p.  32. 


Fig.  oi. — Chronic  Adhesive  Pericarditis. 

The  visceral  layer  shows  marked  thickening  and  opacities  in  places.  Near  the  apex  there 
is  a  large,  thick,  firm  arlhesion  between  the  visceral  and  parietal  layers,  which  presents  the 
evidences  of  prolonged  traction,  and  doubtless  played  a  considerable  part  in  prodviction  of 
cardiac  hypertrophy. 


116  STUDIES  IN  CARDIAC  PATHOLOGY 

Bamberger  was  one  of  the  first  to  point  out  the  frequency  of 
tuberculous  pericarditis,  he  having  stated  that  tuberculosis  was 
second  only  to  rheumatic  fever  as  an  etiologic  factor,  a  view 
which  has  been  reiterated  by  Osier. 

The  occurrence  of  pericarditis  in  nephritis  was  noted  by  Bright 
himself  in  8  per  cent,  of  the  acute  and  6  per  cent,  of  the  chronic 
cases.  This  was  further  emphasized  by  Thomas  Taylor,  who 
among  50  autopsies  found  5  acute  and  7  chronic  cases.  Sibson 
among  285  cases  of  nephritis  at  St.  Mary's  Hospital  found  it  in 
8.8  per  cent.,  and  in  8.17  per  cent,  of  his  1,691  collected  cases. 
Lately  it  has  been  found  in  about  10  per  cent,  of  the  cases  of  in- 
terstitial nephritis. 

The  pericarditis  which  complicates  nephritis  is  generally  a 
terminal  injection.  Among  255  patients  Avho  died  from  cardiac 
or  renal  lesions,  Flexner  found  distinct  evidences  of  terminal 
infection  in  213.  The  bacteriologic  findings  in  the  pericarditis 
cases  were  as  follows :  Micrococcus  lanceolatus,  11;  streptococcus, 
4;  staphylococcus  aureus,  1;  bacillus  pyocyaneus,  1;  bacillus 
influenzae,  1;  mixed  infections,  2;  unidentified  species,  1.^  In 
8  of  the  cases  the  infection  apparently  followed  pneumonia. 

Some  observers  still  believe  that  purely  toxic  cases  may  occur. - 
Thus,  Chattin  found  the  exudate  sterile  in  3  out  of  4  cases 
of  pericarditis  occurring  in  nephritis:  "The  existence  of  asep- 
tic amicrobic  pericarditis  in  certain  cases  of  Bright's  disease 
is  well  established."  Furthermore,  pericarditis  did  not  occur  in 
32  of  Flexner's  cases  of  general  infection  in  nephritis,  whereas  it 
did  occur  in  23  in  which  there  was  a  local  infection.-* 

The  pericarditis  which  occurs  in  nephritis  may  assume  any 
of  the  acute  or  chronic  types.  A  sanguineous  exudate  seems  to 
be  more  common  than  in  the  rheumatic  varietv.     Both  onset 


'  Flexner;  Journal  Experimental  Medicine,  1S96,  p.  1559. 

=  Banti:  Zentralbl.  f.  path.  Anat,,  1894,  p.  461. 

'  Babcock:  Diseases  of  the  Heart  and  Arterial  System,  1903,  p.  45. 


ACUTE    PERICARDITIS  117 

and  course  are  often  insidious,  and  the  termination  is  usually 
rapidly  fatal.  ^ 

Gonococcus  pericarditis,  which  is  sometimes  also  associated  with 
endocarditis,  generally  occurs  only  in  the  severe  and  fatal  cases 
of  gonococcus  septicemia.  In  a  study  of  the  autopsy  records 
from  such  cases  Tyree  found  pericardial  involvement  in  40  per 
cent.;    all  forms  of  exudate  were  encountered.'^ 

Syphilitic  disease  of  the  pericardium  is  probably  less  rare  than 
has  generally  been  supposed.  It  is  generally  a  tertiary  manifes- 
tation which  occurs  secondaril}^  to  myocardial  disease,  as  in  the 
cases  reported  by  Ricord,  Mragek,  Herxheimer,  and  Virchow. 
Well-marked  gummatous  lesions  have  been  reported  only  three 
times  (McPhedran).  Often  the  lesions  appear  as  ordinary  fibrous 
changes.  An  especial  variety  has  been  described  by  Baker,' 
consisting  of  numerous  minute  aneurismal  dilatations  of  the  peri- 
cardial vessels,  together  with  thickening  or  obliteration  of  the  sac. 
It  is  not  unlikely  that  future  studies  based  on  the  finding  of  the 
spirocheta  pallida  will  throw  much  light  on  the  subject.  Wacher 
has  recently  reported  a  case  occurring  as  an  acute  secondary 
manifestation  with  recovery  under  specific  treatment.* 

Laennec  himself  excluded  "milk  spots''  as  not  being  the  results 
of  pericarditis.  Recent  corroboration  of  this  view  is  forthcoming 
as  the  result  of  the  investigations  of  Herxheimer,-^  who  has  de- 
scribed the  microscopic  appearances  as  found  in  a  number  of 
specially  studied  cases.  He  invariably  found  the  endothelial 
layer  of  the  pericardium  destroyed,  and  replaced  by  fibrin,  but 
noted  no  round-cell  infiltration  in  the  underlying  or  surrounding 
tissue.     He  believes,  therefore,  that  milk  patches  have  a  mechanical 

'  H.  B,  Mlyn:  Pennsylvania  Medical  Journal,  1902,  p.  120. 

^Tyrec:  International  Clinics,  Scries  18,  vol.  ii.  (A  considerable  number  of  cases  of 
Konococcus  pericarditis  are  now  on  record,  reference  to  which  may  be  found  in  v.  Hoffmann's 
article,  Centralb.  f.  d.  (Irenzengeb.  der  Med.  u.  Chir.,  1903,  p.  312.) 

^  IJalzer:  Archiv.  d.  .Med.,  18S3,  vi,  93. 

'  Wachor:  Wien.  klin.  Woch.,  1909,  xxii,  p.  96. 

'■'  Hcr.vheimer:  Centralblatt  f.  .all.  Path,  u.  path.  Anal.,  1903,  .\iv,  737. 


118  STUDIES    IN    CARDIAC    PATHOLOGY 

origin,  being  produced  by  pressure  or  friction,  and  not  by  inflam- 
mation. 

These  conclusions  have  been  corroborated  from  both  an 
anatomic  and  an  experimental  standpoint  of  Tsunoda,^  who  likens 
the  mechanism  of  milk  spots  to  the  development  thickening  of 
the  epidermis  on  the  palms  and  soles  as  the  result  of  long-continued 
friction.  He  also  found  that  milk  spots  occurred  with  increasing 
frequency  as  age  advanced. 

Up  to  10  years 8.5  per  cent. 

10  to  20  years 10.0  " 

20  to  30  years 23.0  " 

30  to  40  years 28.0 

40  to  50  years 47.0 

50  to  60  years 54.0  " 

Beyond  60  years 65.0  " 

Primary  endothelial  atrophy  is  followed  bj^  proliferation  of 
the  subendothelial  connective  tissue.  Many  modern  text-books, 
disregarding  these  researches,  still  class  milk  spots  as  the  result 
of  an  antecedent  pericarditis. 

Calcification  of  the  pericardium  sometimes  occurs.  There 
were  two  such  cases  at  the  Philadelphia  Hospital.  The  condition 
seems  to  be  most  commonly  a  sequel  of  a  suppurative  pericarditis. - 

Oberndorfer  has  reported  a  case  of  board-like  pericardial 
thickening  somewhat  in  the  shape  of  a  horseshoe,  measuring  11x4 
cm.,  occurring  in  a  woman  of  seventy  years  and  unassociated  with 
symptoms. 

At  the  Philadelphia  Hospital  an  extreme  case  of  myocardial 
calcification  occurred  in  a  man  of  sixty-five  years,  in  which  the 
process  spread  from  the  anterior  flap  of  the  mitral  valve,  involved 
the  whole  auriculo-ventricular  orifice,  the  wall  of  the  left  ventricle 
just  beneath  the  endocardium,  and  the  interventricular  septum, 
the  heart  weighing  550  gm.  (Phila.  Hospital  Autops}^  Records, 
vol.  xi,  p.  19). 

Actinomj'-cosis  may  produce  plastic  or  suppurative  pericarditis. 

'  Tsunoda:   Frankfurter  Zeit.  f.  Path.,  1909,  iii,  220. 
2  Oberndorfer:   Miinch.  med.  Woch.,  1906,  p.  2081. 


Fiu.  35. — Chronic  Adhesive  Pericarditis. 

J.  T.,  male.     (Pennsylvania  Hospital.     Specimen  46.     Physician:   Dr.  .J.  M.  DaCosta.) 

Clinical  Notes:  Was  admitted  unconscious  and  delirious.  A  diagnosis  of  meningitis 
was  made. 

The  pericardium,  which  was  adherent  to  both  the  epicardium  and  the  surrounding  struc- 
tures, has  been  partially  dissected  back,  and  shows  very  marked  thickening,  and  adhesion. 

The  heart  weighed  1,0.57  gm. 


120  STUDIES  IN  CARDIAC  PATHOLOGY 

Primary  neoplasms  of  the  pericardium  are  rare.  Disease  due  to 
the  cysticercus,  the  echinococcus,  and  trichina  has  been  reported. 
Pathologic  Physiology. — "The  increase  of  pressure  in  the  peri- 
cardial sac  is  an  obstacle  to  the  inflow  of  blood  into  the  heart, 
for  normally  the  inflow  of  blood  into  the  right  auricle  is  greatly 
favored  by  the  difference  in  pressure  inside  and  outside  the  thorax, 
or,  more  strictly  speaking,  outside  the  thorax  and  inside  the  great 
veins  at  their  entrance  into  the  heart.  Since  the  right  auricle 
receives  less  blood  than  normal,  it  can  pass  on  less  blood  to  the 
right  ventricle,  the  right  ventricle  in  its  turn  ejecting  less  blood 
into  the  pulmonary  artery;  the  pulmonary  blood-pressure  falls, 
therefore.  For  the  same  reason — i.  e.,  because  the  pulmonary 
artery  receives  less  blood  than  normal — less  blood  reaches  the 
left  auricle,  and  through  it  the  left  ventricle,  by  way  of  the  pul- 
monary veins.  Since  the  left  ventricle  receives  less  blood,  its 
output  into  the  aorta  is  diminished,  and  diminution  of  output  of 
the  left  ventricle,  unaccompanied  as  in  this  case  by  a  corresponding 
increase  in  the  peripheral  resistance,  is  of  necessity  associated 
with  fall  of  the  aortic  blood-pressure.  "The  venous  blood- 
pressure,  on  the  other  hand,  rises  ....  because  a  new 
condition  has  been  introduced  into  the  circulation  which  disturbs 
the  hitherto  existing  equilibrium  between  the  inflow  into  and  out- 
flow from  the  heart.  It  is  evident,  since  the  aortic  blood-pressure 
is  dependent  upon  the  two  factors,  (a)  output  of  the  heart,  and 
(b)  peripheral  resistance  in  the  arteries,  and  since  the  output  of 
the  heart,  cceteris  -paribus,  depends  entirely  upon  the  inflow  into 
the  heart,  that,  for  the  maintenance  of  a  constant  mean  level  of 
aortic  blood-pressure,  the  inflow  into  the  heart  and  the  output 
must  be  exactly  equal.  But  the  blood  which  constitutes  the 
'inflow'  is  nothing  more  than  that  amount  of  blood  which,  as  the 
result  of  hyperdistention,  passes  from  the  arteries  into  the  veins 
during  cardiac  diastole.  In  other  words,  for  the  maintenance  of  a 
constant  aortic  blood-pressure  the  amount  of  blood  which  passes 
from  arteries  to  veins  during  a  given  cardiac  diastole  must  be 


Fig.  36. — Chronic  Adhesive  Pericarditis. 


iiil)laiiec  of 
w  i  1 1 1  "  ]  leri- 


This  specimen  illustrates  the  "Zuckergusshertz,"  so  called  owing  to  the 
the  exudate  to  the  sugar  icing  on  a  cake.     It  is  generally  met  with  in  associa 
cardial  pseudocirrho.sis  of  the  liver."     (Specimen  from  the  German  Hospital,  I'liilaildphia.) 
See  page  124. 


122  STUDIES  IN  CARDIAC  PATHOLOGY 

exactly  equal  to  the  amount  of  blood  which  has  been  thrown  into 
the  arteries  during  the  previous  cardiac  systole,  and  vice  versa. 

"In  the  case  of  a  dog  into  whose  pericardial  sac  oil  is  injected, 
the  output  of  the  heart  is  diminished,  but  since,  at  the  moment 
before  this  occurred,  the  hyperdistention  of  the  arteries  corre- 
sponded to  a  greater  output,  the  amount  of  blood  which  passed 
from  arteries  to  veins  also  corresponded  to  that  greater  output. 
More  blood,  therefore,  leaves  the  arterial  system  during  any  given 
diastole  than  enters  it  during  the  succeeding  systole;  an  additional 
amount  of  blood,  therefore,  becomes  stored  up  in  the  veins  with 
each  heart's  diastole  until  equilibrium  is  once  more  established, 
gradually  leading  to  the  rise  in  venous  pressure  which  we  have 

noted It  is  this  rise  of  venous  pressure  which  renders 

maintenance  of  the  circulation  possible  under  the  altered  conditions, 
for  it  is  obvious  that  if  the  pericardial  pressure  were  raised  to, 
say,  25  mm.  of  oil,  while  the  pressure  in  the  external  jugular  and 
other  veins  outside  the  thorax  remained  at  their  normal  point, 
no  blood  would  flow  into  the  right  auricle  at  all  and  the  circula- 
tion would  immediatel}'  cease As  it  is,  however,  the 

venous  pressure  rises  with  the  intrapericardial  pressiire,  and  always 
maintains  a  slight  superiorit j^ ;  blood,  therefore,  flows  into  the 
right  auricle,  and  though  the  pressures  in  arteries  and  veins  are 

altered,   the   circulation   goes   on But   the   pressure 

which  can  be  attained  in  the  venous  system  has  a  limit  which 
varies  with  many  factors So  long  as  the  intraperi- 
cardial pressure  is  below  (the  extreme  limit),  the  circulation 
continues,  however  poorly;  but  once  the  intrapericardial  pressure 
reaches  this  point,  all  possibility  of  inflow  from  veins  to  auricles 
ceases  and  circulation  comes  to  a  standstill — the  whole  of  the  blood 
of  the  body  collected  in  the  veins The  heart,  how- 
ever, in  experimental  cases,  for  a  minute  or  thereabouts  continues 
to  contract,  and  if,  during  this  time,  the  intrapericardial  pressure 
be  reduced,  circulation  re-establishes  itself."     (Lazarus  Barlow.^) 

'  Quoted,  McFarland,  Textbook  of  Pathology,  1904,  p.  39S. 


ACUTE    PERICARDITIS  123 

Pericarditis,  although  a  serious  condition,  is  per  se  rarely  the  direct  cause  of 
death.  Brooks  and  Lippincott  only  found  6  such  cases  among  150.  In  86  death 
was  due  to  septic  processes;  17  were  terminal  infections.  In  the  serofibrinous 
cases  death  was  due  to  inflammatory  processes  outside  the  pericardium  as 
follows:  lobar  pneumonia,  30;  bronchopneumonia,  4;  empyema,  1;  acute  en- 
docarditis, 9.  Not  included  in  the  above  there  were  4  cases  of  myocarditis  and 
4  cases  of  acute  tuberculosis.  Pericarditis  greatly  increases  danger  of  endocar- 
ditis during  both  the  acute  and  the  chronic  stages. 

According  to  Theodore  Fisher,  pneumococcus  and  septic  pericarditis  does 
not  produce  cardiac  dilatation  in  the  way  that  the  rheumatic  variety  does,  a  fact 
which  he  explains  as  due  to  the  deleterious  effect  of  the  toxin  of  the  latter  disease 
upon  the  myocardium. 

There  is  some  ground  for  supposing  that  under  normal  conditions  the  peri- 
cardium acts  as  a  support  which  prevents  undue  sudden  cardiac  dilatation,  as 
suggested  by  Hill  and  Barnard,  and  that  an  inflamed  and  softened  and  relaxed 
sac  may  be  a  factor  in  the  production  of  dilatation. 

In  chronic  pericarditis  death  is  seldom  dependent  directly  upon  the  peri- 
cardial lesion.  Of  the  last-named  author's  cases,  5  died  of  cardiac  dilatation, 
1  of  acute  endocarditis,  8  of  lobar  pneumonia,  9  of  sepsis,  1  of  empyema,  9  of 
tuberculosis,  6  of  alcoholism,  4  of  syphilis,  2  of  traumatism,  4  of  non-specific 
myocarditis. 

Until  recently  there  has  been  much  discussion  regarding  the. 
position  of  the  heart  in  cases  of  pericardial  effusion.  A  good  deal 
of  light  has  been  thrown  upon  the  problem  by  Damsch,  Schap- 
oschnikoff^  and  Calvert.-  The  position  of  the  heart  seems  to 
depend  entirely  upon  its  specific  gravity;  in  other  words,  upon  its 
size  and  upon  the  amount  of  blood  it  contains,  and  these  factors, 
in  turn,  depend  upon  the  amount  of  intrapericardial  pressure  and 
the  efficiency  of  compensation.  With  advancing  severity  of  the 
disease  the  heart  contains  less  blood  and  the  pericardial  pressure 
increases.  While  the  heart  is  normal  in  size  it  remains  in  a  normal 
position;  when  it  becomes  smaller,  it  is  pushed  upward  and  back- 
ward, the  apex  being  pushed  slightly  to  the  right. 

'  Schapcschnikoff:  Revue  de  Medecine,  1905,  p.  789. 
^  Calvert:  Bull.  Johns  Hopkins  Hosp.,  Oct.,  1907. 


VIII.   CHRONIC  PERICARDITIS 

Pathogenesis. — If  the  exudate  of  an  acute  pericarditis  is 
absorbed  slowly,  or  if  it  is  mainly  fibrinous  in  character,  adhesions 
are  apt  to  form  as  the  result  of  gradual  organization  of  the  exudate. 
These  adhesions  may  remain  as  localized  circumscribed  white 
areas,  or  they  may,  in  the  form  of  bands  or  threads,  unite  the 
visceral  to  the  parietal  layers,  or  bind  the  external  surface  of  the 
pericardium  to  the  surrounding  mediastinal  tissues.  The  most 
frequent  site  for  such  adhesions  is  on  the  surface  of  the  right 
ventricle;  next  upon  the  auricles;  and  lastly,  upon  the  left 
ventricle.^  (See  Fig.  34.)  Mediastinitis  may  precede  or  follow 
pericarditis.  In  the  former  case  the  infection  generally  spreads  from 
the  bronchial  or  mediastinal  lymph-nodes  or  from  the  lungs  them- 
selves. 

Mediastinitis  has  been  divided  into  three  classes:  (a)  Obhteration  of  the 
pericardial  cavity  with  marked  increase  of  mediastinal  connective  tissue,  with 
or  without  caseation,  (b)  Obliteration  of  the  pericardium  with  extensive  ad- 
hesions to  the  surrounding  structures,  without  much  increase  of  mediastinal 
tissue,     (c)  Mediastinitis  without  pericardial  involvement.''' 

The  most  important  adhesions  are  those  which  occur  between 
the  external  surface  of  the  sac  and  the  surrounding  structures, 
since  it  is  in  these  cases  that  the  heart  is  to  the  greatest  extent 
hampered  and  restricted  in  its  action. 

When  in  addition  to  the  pericardium,  the  mediastinum,  pleurae, 
liver,  and  omentum  are  also  involved,  we  have  what  has  been  de- 
scribed as  pericardial  pseudo-cirrhosis  of  the  liver  (Pick's  disease). 
Both  the  heart  and  the  liver  are  covered  with  a  thick  white  laj^er  of 
inflammatory  product,  so  that  they  have  the  appearance  of  being 
coated  with  "icing,"  hence  the  German  name  "Zuckerguss  Leber 

'  Sicard:  New  York  Med.  Jour.,  1907,  p.  488. 
-  Harris:   Medical  Chronicle,  189.5. 
124 


I'K 


-AcTTE  Fibrinous  Pericarditis. 


A  specimen  from  the  University  of  Pennsylvania  Museum  showing  the  typical  "cor 
villosum,"  or  "shaggy  heart."  (The  entire  heart  could  not  be  better  reproduced  owing  to  the 
difficulty  of  photographing  through  the  convex  surface  of  the  hermetically  sealed  jar  in  which 
the  specimen  was  preserved.) 


126  STUDIES  IN  CARDIAC  PATHOLOGY 

und  Herz."^  This  condition  is  generally  a  part  of  an  extensive 
multiple  serositis,  often  tuberculous  in  origin,  and  is  associated 
with  ascites  and  signs  of  portal  stasis.  Head  collected  55  cases  of 
this  kind,  and  added  4.  He  found  that  one-third  of  the  cases 
occurred  in  persons  under  twenty  years  of  age.  The  commonest 
causal  factor  was  rheumatic  fever,  although  tuberculosis,  pneu- 
monia, nephritis,  and  chorea  were  also  accountable.  Pericardial 
pseudo-cirrhosis  has  been  approximately  reproduced  experimentally, 
by  the  injection  of  iodin  into  the  pericardium.  The  inflammatory 
reaction  which  followed,  by  constricting  the  vena  cava,  produced 
congestion  and  ultimately  cirrhosis  of  the  liver.-     (See  Fig.  36.) 

Clinically,  two  varieties  of  chronic  adhesive  pericarditis  may 
be  distinguished:  (a)  adhesions  followed  by  marked  hypertrophy; 
(6)  complete  obliteration  without  or  with  only  vague  s.ymptoms 
and  with  few  or  no  adhesions  between  the  pericardium  and  the 

'  Study  of  39  cases,  A.  O.  J.  Kelly:  Am.  Jour.  Med.  Sci.,  Jan.,  1903. 
-  Hess:   "Ueber  Stauung  u.  chron.  Entzundung.  i.  d.  Leber  u.  d.  seroesen  Hoelen,"  Mar- 
burg, 1902.     Fletch  and  Schlossberger:  Zeit.  f.  klin.  Med.,  1906,  lix,  1. 


Fig.  38. — Tuberculous  Pericarditis. 

J.  L.,  male,  negro.  (Pennsylvania  Hospital.  Autopsy  No.  277.  Pathologist:  Dr. 
Longcope.) 

Clinical  Notes:  Patient  was  admitted  to  the  surgical  wards  with  a  history  and  physical 
signs  of  appendicitis.     Death  occurred  from  purulent  peritonitis. 

Pathologic  Diagnosis:   Tuberculous  pericarditis,  etc. 

Pericardium:  Both  layers  are  firmly  adherent,  and  have  to  be  dissected  apart.  On 
separation,  they  are  found  to  be  covered  with  small,  more  or  less  discrete,  opaque,  while  eleva- 
tions. Occasionally  these  coalesce  aiid  form  a  lobulated  mass  about  1  cm.  in  rlinmclrr.  the  smaller 
ones  being  of  a  millet-seed  size.  Both  parietal  and  visceral  pericantliini  (in  murli  Ihn-l.-ciied,  the 
former  in  many  places  measuring  5  mm.  On  section  the  entire  pcricunliiim  scctii.^  to  be  com- 
posed ofnodides,  all  of  which  are  very  firm  and  never  umbilicated.  They  do  not  invade  the  myocar- 
dium, which  is  firm  and  dark  reddish-brown  in  color.  The  tissue  between  the  nodules  is  dark 
purplish-red  in  color  and  appears  to  contain  hemorrhages.  There  are  no  nodules  on  the 
external  portion  of  the  visceral  pericardium.  The  left  ventricle  measures  1.5  cm.  in  thickness. 
The  heart  is  somewhat  enlarged;  the  cavities  are  of  fair  size,  and  all  the  valves  are  thin  and 
delicate. 

Microscopic  Examination:  No  especial  changes  are  noted  in  the  myocardium.  The 
pericardium  is  the  seat  of  extensive  tuberculosis.  Covering  the  heart  muscle  there  is  a  thick 
layer  of  granular  tissue,  composed  chiefly  of  epithelioid  cells  and  small  round-cells.  Every- 
where throughout  this  tissue  one  sees  enormous  giant-cells  and  typical  tubercles.  In  the 
granulation  tissue  surrounding  the  tubercles  blood-vessels  are  fairly  numerous.  There  are 
no  areas  of  caseation. 

(Case  reported  by  the  author,  Univ.  of  Pennsylvania  Med.  Bull.,  July,  1904.) 


Fig.  38. 


128  STUDIES  IN  CARDIAC  PATHOLOGY 

surrounding  structures.  The  latter  is  met  with  chiefly  in  males,  is 
independent  of  valvular  lesions,  and  often  occurs  in  individuals 
who  give  no  history  of  antecedent  infections.  The  former  variety, 
which  is  often  seen  in  valvular  disease,  is  associated  with  marked 
hypertrophy  and  dilatation,  and  with  extensive  extrapericardial 
adhesions.  Calcification  of  the  pericardium  sometimes  follows, 
and  myocardial  atrophy  resulting  from  constriction  has  been 
described. 

Fenton '  found  that  "out  of  150  cases  of  adherent  pericarditis,  in  which  the 
cause  of  death  was  specifically  stated  in  the  postmortem  records  to  have  been 
the  direct  result  of  the  heart  lesions,  65  were  found  during  the  first  three  dec- 
ades, and  17  during  the  last  four;  while  where  death  followed  upon  causes 
unconnected  with  the  heart,  13  only  were  found  during  the  last  three  decades, 
and  55  in  the  last  four."  He  also  found  a  history  of  rheumatic  fever  in  most  of 
the  cases  under  thirty  years,  and  in  relatively  few  beyond  this  age;  and,  further, 
that  the  rheumatic  cases  were  generally  the  serious  ones. 

Valvular  disease  was  present  in  91  cases,  absent  in  76;  total,  167.  General 
adhesions  were  found  in  153  cases,  partial  adhesions  in  17;  total,  170. 

The  extent  of  the  adhesion  is  certainly  no  index  of  the  severity 
of  the  lesion,  but  extrapericardial  adhesions  doubtless  play  a  part 
in  the  production  of  hypertrophy  and  dilatation,  as  does  also 
valvular  disease  when  present.  Probably  the  most  important 
etiologic  factor  in  the  production  of  hypertrophj^  and  dilatation  is 
the  myocardial  damage  which  so  commonly  begins  just  beneath 
the  pericardial  lesions,  and  tends  to  progress. 

"Valvular  incompetence  will  exaggerate  the  tendency  to  heart 
failure  by  an  additional  demand  ujDon  cardiac  reserve;  at  the  same 
time  everything  depends  on  the  extent  of  original  damage  sustained 
by  the  muscle."  "Dilatation  takes  place  during  the  acute  and 
subacute  periods  of  the  phase  which  precedes  the  chronic  adhesion. 
In  a  few  mild  cases  it  may  pass  off,  but  in  the  great  majority  it 
does  not,  and  hj^Dcrtrophy  and  external  adhesion  follow;  resulting 
in  a  condition  of  unstable  equilibrium  in  which  the  constant  ten- 
denc3'  is  to  increase  dilatation  and  failure,   owing  partly    to    a 

'Fenton:   Practitioner,  190S,  Ixxxi,  637. 


i'lG.  39. — Tuberculous  Pericaeditis. 
Section  of  the  heart  and  pericardium  from  a  case  of  tuberculous  pericarditis,  sliowing 
complete  obliteration  of  the  sac,  with  thickening  and  caseation.     (Photograph  by  Dr.  Alfred 
Fv.  Allen.) 


130  STUDIES  IN  CARDIAC  PATHOLOGY 

certain  amount  of  embarrassment  to  systole  caused  by  external 
adhesions,  but  mainly  to  permanent  damage  to  the  heart  muscle, 
in  a  manner  resembling  those  cases  of  chronic  cardiac  failure  in 
more  advanced  life"  (Fenton). 

Pathologic  Physiology. — "The  mechanical  effects  upon  the 
circulation  due  to  pericardial  adhesions  may  be  threefold:  (1) 
The  work  of  the  ventricle  is  increased  by  the  tug  upon  the  adhe- 
sions. (2)  The  filling  of  the  heart  may  be  hindered  bj^  strangula- 
tion of  the  vena  cava.  At  each  contraction  the  heart  must  not 
only  drive  out  the  blood,  but  must  pull  on  its  harness  of  adhesions. 
The  additional  work  which  it  thus  has  to  perform  depends  both 
upon  the  tightness  of  the  adhesions  and  upon  the  weight  or  rigidity 
of  the  structures  pulled.  The  latter  factor  depends  upon  the  posi- 
tion of  the  adhesions,  whether  it  is  the  ribs,  pleura,  mediastinum, 
or  the  diaphragm  and  liver  that  are  tugged  upon,  being  greatest 
for  adhesions  to  the  ribs  and  diaphragm.  (3)  The  emptying  of 
the  heart  and  the  flow  through  the  aorta  may,  as  claimed  bj' 
Kussmaul,  be  hindered  by  the  tugging  of  the  adhesions  upon  the 
arch  of  the  aorta.  This  can  readily  be  shown  experimentally  if 
such  traction  be  made  in  a  dog  whose  chest  has  been  opened. 
The  pulse  may  be  made  to  disappear  absolutely  in  spite  of  the  fact 
that  the  heart-rate  remains  unchanged  and  the  heart  dilates  from 
overfilling;  enough  blood  flows  in  from  the  venae  cavse  to  dilate 
the  heart. 

"When  this  additional  work  is  imposed  upon  a  heart  already 
weak,  it  may  succumb  to  the  strain,  and  death  may  occur  with 
all  the  manifestations  of  broken  compensation.  The  importance 
of  adherent  pericardium  in  causing  death  from  heart  disease  is 
shown  by  the  fact  that  it  was  present  in  almost  all  the  cases  of 
Sturges'  series. 

"Usually,  however,  the  ventricles  gradually  recover  from  the 
strain  and  simply  undergo  a  gradual  work  hj^pertrophy  j^ropor- 
tional  to  the  additional  strain,  and  an  additional  amount  of  work 
may  be  done  at  each  systole  sufficient  to  balance  the  amount 


Fk;.  40. — Hemopericardidm. 

The  pericardium  has  been  reflected  to  the  left  and  shows  the  heart  covered  with  a  thick, 
dark,  massive  blood-dot  which  has  resulted  from  the  rupture  of  an  aortic  aneurism  into  the 
pericardium.  The  aorta  is  greatly  dilated  and  its  endocardium  is  roughened  by  extensive 
calcareous  depo.sits.     (Specimen  from  the  Philadcliiliia  Hospital.) 


■132  STUDIES    IN    CARDIAC    PATHOLOGY 

required.  During  exercise,  emotion,  disease,  or  other  strains, 
however,  not  only  the  work  of  the  heart  in  the  circulation  is  in- 
creased, but  with  the  increased  systolic  output  and  systolic  excur- 
sion of  the  walls  the  tug  upon  the  adhesions  is  increased  enor- 
mously, and  the  heart  is  thus  readily  overstrained.  The  heavy 
beating  of  the  heart  under  emotional  excitement  is  especially 
likely  to  bring  this  about. 

"Moreover,  the  process  of  hypertrophy  is  not  a  pure  one. 
With  the  fibrosis  of  the  pericardial  adhesions  outward,  the  process 
of  fibrosis  also  extends  inward  into  the  somewhat  injured  myo- 
cardium, and  this  process  goes  on  progressively  with  each  moment 
of  overstrain  until  the  mj^ofibrosis  cordis  is  advanced  and  the  heart 
failure  complete. 

"The  site  of  the  adhesions  determines  not  only  the  degree  but 
the  character  of  the  heart  failure.  If  the  densest  adhesions  are 
over  the  left  ventricle,  the  effect  is  to  inhibit  the  action  of  the  latter 
alone.  Nature  performs  the  experiment  of  Welch,  and  gives  rise 
to  the  clinical  picture  of  broken  pulmonary  compensation  with 
dyspnea,  cardiac  asthma,  or  pulmonary  edema. 

"If  the  chief  adhesions  are  over  the  right  ventricle,  broken 
systemic  compensation  sets  in,  with  venous  stasis,  tricuspid  insuf- 
ficienc}'^,  enlargement  of  the  liver,  and  collection  of  fluid  at 
various  sites,  but  particularly  in  the  peritoneal  cavity. 

"On  the  other  hand,  the  tugs  of  the  adhesions  on  auricles  and 
ventricles  may  act  as  mechanical  extra  stimuli  and  produce  an 
extrasystolic  arrhythmia,  which  in  itself  hinders  the  circulation." 
(Hirschfelder.) 

Frequency. — Among  2,000  autopsies  at  the  Presbyterian 
Hospital  in  New  York,  Sicard  found  77  cases  of  fibrous  pericarditis 
{314,  per  cent,  of  all  autopsies).  It  was  extensive  in  45,  and  sUght 
in  32  cases.  Mediastinopericarditis  occurred  only  once,  endo- 
carditis was  associated  in  33,  severe  aortic  sclerosis  in  4,  marked 
coronary  sclerosis  in  15,  aneurism  in  4,  chronic  nephritis  in  33, 


I'll;.  41.— K 


Jl'    THIC    .\(litT.' 


Clinical  Notes:  Sudden  death  without  premonitory  symptoms  durinfi  convalescence, 
six  days  after  an  operation  for  hemorrhoids. 

Patholo(;ic  Notes:  Two  and  one-half  centimeters  above  the  attachment  of  the  aortic 
valve.s  there  is  a  rough,  uliijhlly  nhaggy  looking  tear  running  direcUy  across  the  aorta.  It  is  2  cm. 
in  length  and  leads  directly  from  a  small  aneurismal  pouch  into  the  pericardial  cavity.  The 
.surface  of  the  aorta  along  the  ascending  arch  shows  small,  scattered,  yellowish  nodules.  (Spec- 
imen from  the  Pennsylvania  Hospital.     Pathologist:   Dr.  G.  C.  Robinson.) 


134  STUDIES  IN  CARDIAC  PATHOLOGY 

tuberculosis  in  9.  Leudet  in  1,002  autopsies  found  partial  adhesion 
in  5  per  cent.,  total  adhesion  in  2.5  per  cent. 

Congenital  defects  of  the  pericardium  are  very  rare.  The  sac 
may  be  wanting  in  acardiac  monsters,  and  sometimes  even  when 
the  heart  is  present,  or  it  may  only  partially  cover  the  heart. 
Ebstein  collected  32  cases  of  congenital  absence,  and  found  that 
the  clinical  picture  in  many  respects  resembled  the  "movable 
heart."' 

The  following  pericardial  lesions  were  encountered  among  9,940  autopsies: 

Philadelphia  Hospital        Pennsylvania  Hospital 

Carcinoma  (metastatic) 3  0 

Sarcoma  (metastatic) 5  1 

Calcificition 7  1 

Rupture  of  abscess  into 2  0 

Ctumma 1  0 

Rupture  of  aneurism  into 2 

Neither  the  sarcomas  nor  the  carcinomas  enumerated  in  the 
foregoing  statistics  were  primary.  In  the  case  of  tumors  origi- 
nating in  the  heart,  pericardial  involvement  is  very  rare.  Among 
61  cases  of  cardiac  neoplasms  Schoepplcr'-  found  the  pericardium 
involved  only  once. 

Clinical  Considerations. — The  existence  of  primary  pericarditis 
is  no  longer  admitted.  Whenever  a  true  inflammation  of  this  sac 
occurs,  it  is  due  to  an  antecedent  infection  of  the  blood-stream, 
lymphatics,  or  contiguous  structures.  The  cases  which  were  at 
one  time  believed  to  have  a  toxic  origin  are  now  known  to  be 
infections.  "Milk  spots"  have  a  mechanical  origin  which  is  of 
a  non-inflammatory  nature. 

No  serious  cardiac  lesion  is  so  frequently  overlooked.  Cabot  ^ 
found  that  of  54  cases  of  acute  pericarditis  at  the  Massachu- 
setts General  Hospital,  70  per  cent,  were  not  recognized  ante 
mortem.  Any  one  who  is  familiar  with  autopsy  records  will 
realize  that  a  similar  state  of  affairs  is  the  general  rule  elsewhere, 

'  Ebstein:   Mtinch.  med.  Woch.,  March  8,  1910. 

-  Schoeppler:   Miinch.  med.  Woch.,  1906,  hii,  No.  45. 

=  Cabot:  Jour.  Am.  Med.  Assoc,  1910,  p.  134:3. 


CHRONIC    PERICARDITIS  135 

owing  to  the  fact  that  the  onset  of  a  pericarditis  is  general!}' 
insidious,  and  that  such  symptoms  and  physical  signs  as  it  does 
present  are  usually  completely  overshadowed  by  the  conditions 
which  it  complicates.  The  obvious  lesson  to  be  learned,  there- 
fore, is  to  look  actively  for  signs  of  pericardial  involvement  in 
conditions  such  as  pneumonia,  rheumatic  fever,  nephritis,  tuber- 
culosis, emp3'ema,  etc.,  in  which  it  so  often  occurs. 


IX.  CARDIAC  HYPERTROPHY 

DIMENSIONS  OF  THE  NORMAL  HEART.— (Bizol.) 

Males  Females 

(Meters)  (Meters) 

Length  of  the  heart 0.097  0.092 

Breadth  of  the  heart 0.107  0.099 

Thickness  of  the  heart 0.038  0.031 

Length  of  the  left  ventricle 0.066  0.072 

Breadth  of  the  left  ventricle 0.119  0.104 

Length  of  the  right  ventricle •.  . .  0.084  0.075 

Breadth  of  the  right  ventricle 0.188  0.172 

Thickness  of  the  Walls  of  the  Left  Ventricle: 

At  the  base 0.010  0.009 

At  the  middle 0.011  0.010 

Near  the  apex 0.008  0.007 

Thickness  of  the  Septum  Ventriculorum: 

At  the  middle 0.011  0.009 

Thickness  of  the  Walls  of  the  Right  Ventricle: 

Base 0.004  0.003 

At  the  middle 0.003  0.002 

Near  the  apex 0.002  0.002 

Breadth  of  the  Auriculo-Ventricular  Orifices: 

Left  ventricle 0.100  0.091 

Right  ventricle 0.122  0.106 

Breadth  of  the  origin  of  the  aorta  (above  the 

valves) 0.069  0.063 

Breadth  of  the  origin  of  the  pulmonary  artery  0.071  0.066 

The  heart  of  an  adult  man  averages  300  gm. ;  of  a  woman,  250  gm. 
The  size  of  the  cardiac  orifices  is  given  by  Perls  as  follows : 

Under  Between  Forty  .\nd  Over 

Forty  Ye.vrs.  Fifty  Ye.\rs.  Fifty  Years. 

Aortic  orifice,  cardiac 70.9  mm.  74.6  mm.  74.3  mm. 

Aortic  orifice,  arterial 63.5     "  72.2     "  80.1     " 

Pulmonary  orifice,  cardiac 81.5     "  84.9     "  85.7     " 

Pulmonary  orifice,  arterial 71.9     "  74.6     "  81.3     " 

Mitral  orifice,  periphery 102.5     "  105.1     "  102.0     " 

Tricuspid  orifioe,  periphery 121.0     "  122.0     "  122.8     " 

It  appears,  therefore,  that  there  is  a  difference  not  only  in  the  size  of  the 
aortic  and  pulmonary  orifices,  depending  upon  whether  they  are  measured  at 
the  opening  of  the  heart  proper  or  at  the  attachment  of  the  semilunar  valves, 
but  also  that  the  proportion  of  these  two  dimensions  to  each  other  is  directly 
reversed  before  and  after  forty  years  of  age.  "In  middle  Hfe  the  unfolded  valves 
take  up  a  greater  space  than  that  which  they  must  actually  cover,  while  in  old 

136 


CHRONIC    PERICARDITIS  137 

age  they  generally  take  up  a  smaller  space."  These  facts  help  to  explain  the 
greater  frequency  of  insufficient  valves  in  old  age.'-  This  increase  in  the  size 
of  the  vessels  is  due  to  diminished  elasticity  of  arteriosclerotic  vascular  walls. 
Arteriosclerotic  aortae  are  often  overlooked  because  they  simply  show  dilatation, 
without  sclerotic  patches.'' 

The  size  of  the  heart  is  proportionate  to  bodily  weight,^  and 
to  a  lesser  extent  to  stature.  In  adolescents,  in  corpulent  subjects, 
and  in  women  the  size  of  the  heart  is  relatively  smaller  than  in 
adult  men  of  the  same  proportions,  especially  those  with  good 
muscular  development.  It  also  increases  with  age,  but  enlarge- 
ment to  the  left,  as  shown  by  percussion  or  b.y  the  orthodiagram, 
is  not  solely  due  to  hypertrophy,  but  also  to  the  fact  that  in  ad- 
vanced years  the  organ  lies  more  to  the  left.  The  dome  of  the 
diaphragm  sinks,  and  with  this  descent  the  heart  moves  downward 
and  to  the  left. 

In  early  life  the  upper  cardiac  border  reaches  the  second,  and 
in  adult  life  the  third,  costal  interspace.  The  diaphragm  being 
more  highly  placed  in  women,  the  heart  is  correspondingly  higher 
in  position.  The  lower  cardiac  border  is  found  in  52  per  cent,  of 
male  adults  at  the  angle  of  the  costosternal  junction,  in  women 
in  70  per  cent.  (Muller,  Hirsch,  Dietlen).^  In  men  the  weight 
of  the  heart  to  the  whole  body  is  about  1  to  170;  in  women  it  is 
1  to  183. 

Occurrence. — Hypertrophy  of  the  heart  consists  of  an  increase 
in  either  the  number  or  the  size  of  the  muscle-cells,  or  both. 
Practically,  however,  hypertrophy  of  the  heart  as  generally  seen 
is  in  part  also  due  to  an  increased  amount  of  connective  tissue,  fat, 
and  blood-vessels.  It  is  directly  due  to  an  increased  demand  for 
work,  arising  either  within  or  without  the  heart — valvular  lesions, 

'  Quoted,  Ro.senstein:  Ziemssen's  Cylcop.  of  Med.,  vi,  p.  13. 

^  Scheel:  "Study  of  .500  Autopsies,"  Norsk  Mag.  f.  Laegevidenskaben,  June,  1907. 

'  In  animals  which  have  been  starved  the  heart  diminishes  in  proportion  to  the  loss  of 
bodily  weight,  and  regains  its  original  size  (as  shown  by  the  orthodiagram)  when  feeding  is 
resumed.  This  decrease  in  size  seems  to  be  due  partly  to  actual  loss  of  substance,  and  partly 
to  a  decreased  volume  of  blood.  One  animal  in  the  course  of  nine  days  lost  .'31  per  cent,  of  its 
total  blood.     (SchielTcr:  Dcut.  Arch.  f.  kHn.  Med.,  1907,  xcii,  Dec.  28.) 

*  Muller:  Die  MassHnverhaeltnisse  des  monschlichen  Ilerzens,  Berlin,  1S7S;.  Ilirsch: 
Deut.  .Xrch.  f.  klin.  Med.,  1899,  p.  .597.     Dictlen:   Dcut.  Arcli.  f.  l<Hii.  Med.,  Orl.  24,  1906. 


138  STUDIES  IN  CARDIAC  PATHOLOGY 

congenital  defects,  pericarditis,  scoliosis,  cardiac  thrombosis, 
aneurisms,  neoplasms  of  the  mediastinum,  arteriosclerosis,  gout, 
lead-poisoning,  etc.  Although  hypertrophy  may  affect  only 
one  chamber,  this  is  unusual.  Hypertrophy  has  also  been  as- 
cribed to  defective  innervation.  Although  a  common  cause  of 
hypertrophy  is  arterial  hypertension,  yet  the  continued  rapidity 
of  action  which  occurs  over  years  of  time  in  hypotension  may 
produce  a  similar  result.  Thus  we  see  hypertrophy  associated 
with  hyperthyroidism. 

Systematic  writers  have  been  wont  to  recognize  three  types  of 
cardiac  hypertrophy:  (1)  Simple  enlargement,  without  change 
in  the  size  of  the  cavities;    (2)  concentric  enlargement,  with  dimi- 


FiG.  42. — Concentric  Cardiac  Hypertrophy. 

W.  B.,  negro,  laborer,  aged  forty-five  years.  (Pennsylvania  Hospital.  No.  1442  (1908). 
Physician:   Dr.  A.  Newlin.     Pathologist;  Dr.  Krumbhaar.) 

Clinical  Notes:  Delicate  as  a  child.  Healthy  at  eighteen  years.  Hard  worker. 
Alcohol  and  tobacco  to  excess.  Syphilis  probably.  Six  months  ago  nausea  and  vomiting, 
with  increasing  headaches.     Brought  to  hospital  unconscious  and  soon  died. 

Pathologic  Diagnosis:  Tumor  of  the  pituitary  body,  etc.  Acute  mitral  endocarditis. 
Chronic  mitral  and  aortic  endocarditis — concentric  cardiac  hypertrophy.  Arteriosclerosis  of  the 
aorta,  etc. 

Pericardium  contains  10  c.c.  of  clear  fluid;  no  adhesions. 

Heart:  Weighs  530  gm.,  enlarged  and  firm.  Normal  color.  Epicardium  grayish,  and 
diffusely  thickened.  In  spots,  dense  white,  opaque  areas,  which  cut  with  resistance.  Epi- 
cardial  fat  increased.  Epicardium  over  right  auricle  tessellated  with  slight  raised,  grayish, 
pin-point  nodules.  Right  ventricle  6  to  10  mm.  Auricular  and  pulmonary  valves  normal. 
Left  heart  empty,  its  musculature  enormously  increased;  measures  IS  to  SB  mm.  Its  cavity 
smaller  than  would  he  expected.  Endocardium  smooth  and  glistening,  though  on  the  septal  wall 
some  of  the  vessels  seem  dilated.  Mitral  orifice  10.5  cm.  and  shows,  especially  on  the  anterior 
leaflet,  diffuse  fibrous  plaques.  Along  the  whole  line  of  closure  are  minute  grayish  vegetations  of 
pin-point  size.  Aortic  orifice  7  cm.;  shows  some  fibrous  thickening  along  the  base  of  the  leaflets, 
the  line  of  closure  being  normal.  Aorta:  nodular  yellowish  thickenings,  and  a  certain  amount  of 
branching  contractions  like  the  willow-tree  type  of  sclerosis.  Coronary  arteries:  except  at  the 
origin  are  normal. 

Microscopic  Diagnosis:  Chronic  interstitial  myocarditis.  The  muscle  shows  well- 
marked  stria;,  and  not  much  pigment  about  the  nuclei.  The  fibers,  especially  on  cross-section, 
are  much  shrunken  from  the  sarcolemma,  and  occasionally  extensive  areas  with  large  rectangular 
nuclei  are  found.  Interstitial  tissue  is  diffusely  thickened,  especially  about  the  blood-vessels, 
whose  walls  are  also  thickened.  At  the  edges  of  the  fibrosed  areas  the  muscle-fibers  are  often 
vacuolated,  while  others  are  small  and  shrunken,  having  lost  their  striae.  The  process  is  more 
advanced  and  extensive  in  the  papillary  muscles  than  in  the  ventricular  wall.  Sections  of  the 
mitral  valve  show  that  both  the  ventricular  and  the  auricular  endocardium  are  thickened,  espe- 
cially the  former.  In  some  areas  the  endothelial  layer  is  broken,  and  fibrous  tissue  directly 
continuous  with  the  adherent  masses  of  fibrin  is  seen,  which  occasionally  includes  red  and 
white  blood-cells.  There  is  considerable  coarse  fibrous  tissue  between  the  two  endocardial 
layers. 


Fig.  42. 


140  STUDIES    IN    CARDIAC    PATHOLOGY 

nution  in  the  size  of  the  cavities;  (3)  eccentric  enlargement,  with 
enlargement  in  the  size  of  the  cavities  (also  spoken  of  as  hj^per- 
trophic  dilatation).  The  second  type,  regarding  the  existence 
of  which  there  is  some  difference  of  opinion,  may  be  simulated  if 
death  occurs  during  sj^stole.  (See  Figs.  43,  44,  45.)  In  such  a 
case  prolonged  immersion  in  water  will  bring  about  a  relaxation 
of  the  heart  muscle. 

Pathogenesis. — Excessive  demand  for  work  on  the  part  of 
the  heart  calls  forth  the  latent  reserve  force  which  every  normal 
heart  possesses,  and  which  represents  the  surplus  energy  which 
has  been  stored  up  under  periods  of  rest.  When  the  demand  for 
increased  work  becomes  constant,  hypertrophic  changes  are  brought 
about.  If  the  demands  exceed  the  limit  of  the  field  of  response, 
or  the  nutritional  possibilities,  dilatation  occurs. 

As  has  been  intimated  above,  the  term  "concentric  hyper- 
trophy" is  justly  falling  into  disuse  because  there  is  no  actual 
diminution  in  the  size  of  the  chambers  in  such  cases.  When 
hypertrophy  is  due  to  an  obstruction  to  the  outflow  of  blood, 
simple  hypertrophy^  is  induced;  when  it  arises  from  diastolic 
overfilling,  hypertrophy  and  dilatation  occur.  This  does  not 
result  from  mere  stretching  of  the  muscle-fibers  (because  even 
with  increased  diastolic  filling  there  is  no  increase  in  muscular 
tension),  but  owing  to  the  fundamental  attribute  of  the  heart 
muscle,  by  virtue  of  which  every  contraction  is  maximal.  Although 
the  contraction  time  is  prolonged  when  obstruction  to  outflow  or 
increased  diastolic  filling  occur,  this  increase  is  not  in  proportion 
to  the  amount  of  the  hindrance  or  of  the  overfilling  imposed 
(Romberg). 

Hypertrophy  affects  only  such  parts  of  the  heart  muscle  as 
are  actually  called  upon  to  do  extra  work.  An  associated  or 
sympathetic  hypertrophy,  or  one  due  merely  to  increased  nutri- 
tional advantages,  is  never  found  (Romberg).  Atrophy  and  hy- 
pertrophy of  different  chambers  of  the  same  heart  are  often 
encountered,  as  has  been  shown  by  Hirsch.     Hypertrophy  of  the 


1  ii..  4o. — Vi^KTK'AL  Section  of  the  Thorax.     (See  also  Fig.  44. J 

Figs.  43  and  44  show  what  appears  to  be  a  most  extraordinary  concentric  hypertrophy  of 
Ike  left  ventricle.  The  walls  of  this  chamber  are  enormously  thickened  and  the  chamber  itself 
almo.st  obliterated  as  the  result  of  it.  This  specimen  was  found  among  the  anatomic  material 
at  the  University  of  Pennsylvania.  Nothing  is  known  regarding  the  history  of  the  individual, 
but  it  is  inconceivable  that  such  an  extreme  concentric  hypertrophy  should  have  developed 
without  more  adequate  cause  than  is  demonstrable.  The  aorta  above  the  valves  shows  the 
results  of  a  syphilitic  aortitis,  but  the  valve.s  themselves  are  only  moderately  thickened.  We 
have  a.s.sumftd,  therefore,  that  an  explanation  must  be  sought  in  the  fact  that  the  heart  ceased 
HCtiriK  ill  .systole.      ('Sfctions  prepared  by  Dr.  flcorgc  I'V'lterolf.) 


142  STUDIES  IN  CARDIAC  PATHOLOGY 

conducting  fibers — auriculo-ventricular  bundle,  etc. — does  not 
occur  (Aschoff  and  Tawara).' 

The  mechanism  by  which  hypertrophy  is  produced  probably 
varies;  the  most  important  being  that  due  to  increased  intra- 
cardiac pressure.  This  factor  normallj^  acts  as  a  stimulus  to 
contraction,  as  has  been  shown  by  v.  Frey."  Before  birth  the 
walls  of  the  two  ventricles  are  of  equal  thickness,  but  afterward, 
when  much  greater  work  is  demanded  of  the  left  ventricle,  its 
walls  become  much  thicker  than  those  of  the  right.  That  this 
pressure  or  stretching  hypertrophy  is  independent  of  nervous 
influences  seems  likely  from  the  investigations  of  Rieder.-* 

A  considerable  number  of  cases  of  hypertrophy  are  due  to 
chemical  factors.  In  this  group  are  included  adrenalin,  and 
metabolic  products  of  more  or  less  undetermined  composition, 
such  as  occur  in  renal  disease  and  intestinal  autointoxication. 

As  opposed  to  a  mechanical  origin  of  cardiac  hypertrophy 
we  have  the  "irritation"  hypothesis  of  v.  Dusch,  it  being  assumed 
that  increase  of  intracardiac  pressure  by  stimulation  of  the  cardiac 
nerves  and  ganglia  produces  an  increased  force  of  contraction, 
and  this  in  turn  hypertrophy.* 

Still  another  non-chemical  explanation  has  been  offered  by 
Albrecht,^  who  discards  the  internal  pressure  or  nervous  hjq^othesis 
as  untenable,  and  regards  hypertrophy  as  the  result  of  a  chronic 
proliferative  myocarditis — an  inflammatory  hyperplasia — which 
exists  not  as  an  isolated  manifestation,  but  as  an  attribute  of  a 
chronic  process  which  is  often  associated  with,  it  may  be,  nephritis, 
valvular  disease,  etc.  Other  varieties  of  hypertrophy  not  ex- 
plainable on  this  basis  are  assumed  to  result  from  chemical  and 
bacterial  and  metabolic  toxins. 

1  This  statement  is  also  corroborated  by  Moenkeberg,  "  Untersuchungen  li.  d.  Atrio-ven- 
trikular  Biindel  im  menschliclien  Herzen,"  1909. 

2  Frey:  Deut.  Arch.  f.  Idin.  Med.,  1889,  xlvi,  p.  .398. 

3  Rieder:   Arch.  f.  Win.  Med.,  1895. 

■"Asch;  Zur  Hypertrophie  d.  Quergestreiften  Muskeln,  speziel  des  Herzmuskels',  Berlin, 
1906. 

^Albrecht:  Der  Herzmuskel  u.  s.  Bcdeutung  f.  Physiol.,  Pathol,  u.  Klinik  d.  Herzens, 
Berlin,  1903. 


Fifi,  44. — Vertical  Section  of  the  Thouax.     (Sep  doscriptivc  legend  for  rig.  4'A.) 


144  STUDIES  IN  CARDIAC  PATHOLOGY 

It  has  been  found  that  chronic  nephritis  with  hypertension  is  very  fre- 
quently associated  with  enlargement  of  the  suprarenal  gland,'  and,  further,  that 
in  some  cases  an  abnormally  large  amount  of  the  secretion  of  this  gland  can  be 
demonstrated  in  the  circulating  blood.  Again,  it  appears  that  removal  of  the 
suprarenals  produces  a  fall  of  blood-pressure,  and  that  the  serum  of  clogs  thus 
treated  has  a  hypotensive  action. - 

Finallj^,  nervous  factors  are  probably  responsible  for  hyper- 
trophy in  a  certain  number  of  cases.  Thus,  for  instance,  neurotic 
individuals  with  a  permanently  rapid  pulse-rate  often  develop 
minor  grades  of  hypertrophy. 

While  cardiac  hypertrophy  is  most  common  in  the  sulDJects  of  aortic  disease, 
of  interstitial  nephritis,  and  in  the  sons  of  heavy  toil,  it  is  by  no  means  a  negligible 
factor  exclusive  of  the  just  mentioned  conditions.  Lubenau^  in  the  sanatorium 
for  heart  diseases  at  Beehtz,  from  which  valvular  diseases  are  excluded,  found 
that  40  per  cent,  of  the  admissions  were  on  account  of  "idiopathic  hypertrophy," 
35  per  cent,  were  carchac  neuroses,  and  10  per  cent,  primary  cardiac  weak- 
ness. 

When  the  left  ventricle  is  hypertrophied,  the  arterial  system  is  subjected  to 
violent  alterations  in  pressure,  which  produce  minute  ruptures  in  the  vascular 
coats ;  this  leads  to  fibrosis,  and  ultimately  to  an  arteriosclerosis,  which  in  turn 
demands  a  greater  hypertrophy,  and  thus  a  vicious  circle  is  established. 

Since  increased  work  on  the  part  of  the  heart  produces  hypertrophy,  animals 
which  are  fleet  of  foot — deers,  hares — have  larger  hearts  than  less  active  animals 
of  an  equal  size.  The  wild  rabbit  has  a  larger  heart  than  his  tame  cousin.  The 
same  law  holds  good  for  birds  of  long  flight."  Animals  of  the  same  size  and 
breed  which  are  forced  to  exercise,  develop  larger  hearts  than  the  controls  which 
are  prevented  from  exercising."  We  also  know  that  not  only  the  left,  but  also 
the  right  ventricle  hypertrophies  in  these  cases,  due  apparently  to  increased 
pressure  in  the  pulmonary  circulation  during  exercise,  since  it  has  been  shown 
that  activity  produces  a  physiologic  emphysema,  and  this  in  turn  increases 
tension  in  the  pulmonary  capillaries.  Athletes,  especially  those  accustomed  to 
prolonged  contests,  such  as  rowing,  bicycling,'^  and  long-distance  running,  gen- 
erally develop  more  or  less  hypertrophy.  They  are  said  to  be  two  and  one-half 
times  as  subject  to  carchac  chseases  as  other  people.'  Participation  in  record- 
breaking  feats  has  been  shown  to  be  especially  harmful.^ 

1  Philpot:  Quart.  Jour.  Med.,  Oct.,  1909. 

^  Reneau:  Thftse  de  Lyon,  1909. 

■'  Lubenau:  Zeit.  f.  klin.  Med.,  1906,  Ix,  p.  134. 

•'  Grober:  Deut.  Arch.  f.  klin.  Med.,  1907,  xoi,  p.  .502. 

^  Kulbs:  Munch.  Kongr.  f.  inn.  Med.,  April,  1906. 

'•  Sliieffer:  Deut.  Arch.  f.  klin.  Med.,  Ixxxix,  604. 

'  Hutchinson,  quoted  Davy:  Lancet,  Feb.  16,  1907. 

SSeUg:   Mediz.  Klinik,  March  29,  1908. 


Fig.  45. — Cardiac  Hypertrophy. 

A  specimen  from  the  Museum  of  the  University  of  Pennsylvania,  illustrating  the  type 
known  as  "concentric  hypertrophy."  The  wall  of  the  left  ventricle  shows  an  enormous  degree 
of  thickening;  the  cavity  has  apparently  not  enlarged  in  proportion.  The  aorta  shows  well- 
marked  atheroma  ami  calcification  .-ibout  the  sinus  of  Valsalva. 


146  STUDIES  IN  CARDIAC  PATHOLOGY 

A  hypertrophied  heart  is  never  as  efficient  as  a  ndrmal  organ, 
because  associated  with  its  increase  in  size  there  has  been  no 
corresponding  increase  in  the  size  or  number  of  its  ganglion-cells, 
nerve-cells,  or  nutritional  possibilities.  Although  the  existence  of 
a  pure  "work  hypertrophy"  may  be  accepted  as  proved,  despite 
the  denial  of  its  existence  by  some  well-known  clinicians,  neverthe- 
less hypertrophies  of  this  sort  never  attain  the  enormous  dimen- 
sions which  are  met  with  in  the  hypertrophy  of  disease.  An 
increase  of  50  odd  per  cent,  may  be  produced  by  the  former,  and 
an  increase  of  200  or  300  per  cent,  may  occur  in  the  latter.  Thus, 
some  enormous  hypertrophies  have  been  recorded — 1300  gm. 
(Jackson^),  1700  gm.  (Osier),  2500  gm.  (Norristown  Hospital). 
Among  32  arteriosclerotic  hearts  studied  by  Jackson,  only  4 
weighed  less  than  400  gm. 

Great  cardiac  enlargement  naturally  takes  up  considerable 
intrathoracic  space.  When  there  is  insufficient  room,  we  see 
bulging  of  the  precordial  ribs  and  compression  of  the  lungs.  How 
great  this  compression  may  be,  is  shown  in  a  case  at  the  Philadelphia 
Hospital  in  the  service  of  Dr.  Lloyd,  in  which  actual  erosion  of 
the  thoracic  vertebrae  was  thus  produced.^  Lack  of  space,  if 
of  sufficient  degree,  may  mechanically  interfere  with  heart  action 
and  be  the  direct  cause  of  cardiac  symptoms.  This  fact  has  been 
especially  dwelt  upon  by  Herz.-' 

'  Jackson:  Boston  Med.  and  Surg.  Jour.,  1896. 

2  Philadelphia  Hospital  Autopsy  Records,  vol.  x,  p.  17.     (April  4, 1897.) 

'  Herz:  Wien.  med.  Woch.,  1908,  xxxiii,  397. 

Fig.  46. — Sagittal  Section  op  the  Thorax.  (See  also  Figs.  47  and  48.) 
Figs.  46,  47,  and  48  demonstrate  how  little  room  for  expansion  there  is  for  the  heart 
between  the  vertebral  column,  and  the  anterior  thoracic  wall.  Displacement  to  the  right  is 
impracticable,  since  the  antero-posterior  thoracic  dimensions  are  smallest  in  the  median  hne. 
Movement  to  the  left  is  hindered  by  the  increasing  convexity  of  the  ribs.  If  any  displacement 
takes  place,  therefore,  it  must  be  backward  and  downward.  When  the  possibility  of  motion 
in  these  directions  is  exhausted,  a  squeezing  of  the  heart  must  occur.  It  is  plainly  evident  that 
such  a  state  of  crowding,  whether  it  results  from  enlargement  of  the  heart  or  of  the  lungs 
(pericardial  effusion)  or  from  deformity  of  the  chest — empyema,  etc. — must  have  a  deleterious 
effect  not  only  on  the  functionation  but  also  upon  the  nutrition  of  the  heart.  The  most 
striking  effects  which  result  from  diminished  intrathoracic  space  are  noted  in  cases  of  valvu- 
lar insufficiency,  especially  when  associated  with  dilatation  and  myocarditis  (Herz) .  (Sections 
from  the  Laboratory  of  Anatomy  of  the  University  of  Pennsylvania,  Dr.  George  Fetterolf.) 


Bight  pulmonarj'^  arterj- 


Left  superior  pulmon- 
ary vein 
I>eft  auricular  appendix 
Left  inf.  pulm.  vein 

Left  auricle 


Mitral  valve  (anterio 


■  Aortic'Ieaflets 


,  Left  ventricle 
.  Kight  \'-entricIe 


Via.  40. 


148  STUDIES    IN    CARDIAC    PATHOLOGY 

Probably  a  part  of  the  dyspnea  seen  in  high  grades  of  pulmonary  emphysema 
is  due  to  this  crowding  of  the  heart.  The  great  lessening  of  dyspnea  in  cardiac 
patients  by  the  simple  procedure  of  propping  them  up  in  bed,  so  that  with  lower- 
ing of  the  diaphragm  the  heart  is  afforded  more  room,  is  another  example  of  the 
importance  of  external  pressure. 

This  is  well  illustrated  in  Figs.  43  and  44,  a  glance  at  which 
will  show  how  snugly  the  heart  is  fitted  in  between  the  lungs  and 
diaphragm.  1 

Exclusive  of  valvular  lesions,  chronic  nephritis  is  perhaps  the 
most  frequent  cause  of  cardiac  hypertrophy.  The  exact  modus 
operandi  by  virtue  of  which  it  occurs  is  still  unsettled.  In  many 
cases  arterial  hypertension  seems  to  be  accountable  for  the  con- 
dition, but  this  factor,  while  usually,  is  not  invariably,  present. 
Then,  again,  we  have  still  to  learn  the  cause  of  such  hypertension, 
whether  it  is  reflex  or  toxic,  whether  it  is  due  to  arteriosclerosis, 
especially  of  the  splanchnics  or  the  renal  arteries;  whether  it  is 
due  to  overactivity  of  the  adrenals,  and  if  so,  why  such  an  over- 
secretion  occurs.  The  hypertrophic  changes  are  apparently  closely 
associated  with  contraction  of  the  smaller  arteries,  which,  in 
turn,  seems  to  be  due  to  a  toxic  factor. 

The  importance  of  arteriosclerosis  or  constriction  of  the  splanch- 
nic area  as  a  cause  of  hypertension  and  cardiac  hypertrophy, 
which  was  prominently  brought  to  the  fore  through  the  investi- 
gations of  Hasenfeld-  and  Hirsch,^  and  widely  accepted,  has 
apparently  been  overestimated.  Marchand,"  as  well  as  Longcope 
and  McClintock,=  were  unable  to  corroborate  the  above-mentioned 
observations.  Neither  experimentally  or  at  autopsy  could  the 
last-mentioned  investigators  find  any  definite  association  between 
cardiac  hypertrophy  and  sclerosis  of  the  abdominal  aorta  or  the 
splanchnic  vascular  domain. 

Cystic  kidneys  and  hydronephrosis  are  often  associated  with 

'  These  sections  were  prepared  by  Dr.  George  Fetterolf . 
=  Hasenfeld:   Deut.  Arch.  f.  klin.  Med.,  1897,  p.  193. 
'Hirsch:   Ibid.,  1899,  p.  579. 

'  Marchand:  Verhandl.  d.  Kong.  f.  inn.  Med.,  1904,  p.  60. 
'  Longcope  and  McClintock:  Arch.  Int.  Med.,  1910,  p.  439. 


Superior  vena  cava 


Right  auricle 
Coronary  sinus 


Tricuspid  valve 


Via.  47.— SAr;irrAr>  Skction  of  thk  'J'hohax.     fSco  (Icsrriplivf  legend  under  Kifr.  46.) 


150  STUDIES  IN  CARDIAC  PATHOLOGY 

cardiac  hypertrophy.  Myocardial  changes  and  disease  of  the 
coronary  arteries  are  often  relatively  slight  in  nephritis,  and  death 
from  heart  failure  is  more  frequent  in  secondary  than  in  primary 
nephritis.^ 

It  was  formerly  taught  that  the  hypertrophy  which  occurs 
in  chronic  nephritis,  and  even  in  acute  nephritis  if  its  duration 
exceeds  four  weeks,-  affected  chiefly,  if  not  entirely,  the  left 
ventricle.  Careful  examinations  by  MuUer's  method  have  shown 
that  all  the  cardiac  chambers  are  affected''  in  82  per  cent,  of  the 
cases.  It  is  true,  however,  that  the  left  ventricle  shows  the  most 
pronounced  changes,  and  that  right-sided  enlargement  appears 
to  be  definitely  a  sequel  (Paessler) .  The  hypertrophy  is  generally 
regarded  as  due  to  increased  work  of  the  left  ventricle  in  over- 
coming abnormal  resistance.  With  a  normal  blood-pressure  the 
heart  handles  about  10  pounds  of  blood  per  minute,  and  with 
hypertension  this  work  may  readily  be  doubled.  The  nephritis 
in  which  interstitial  changes  preponderate  is  the  type  in  which 
cardiac  hypertrophy  most  frequently  occurs,  although  cases  of 
this  type  are  sometimes  seen  without  either  hypertension  or 
cardiac  hypertrophy.  Some  cases  of  diffuse  nephritis  are  ac- 
companied by  hypertrophy,  although  this  is  unusual.  Hyper- 
trophy is  said  never  to  occur  in  amyloid  renal  disease.  It  may, 
according  to  Cohnheim,  follow  obstruction  of  the  ureter. 

The  interrelationship  between  disease  of  the  heart,  the  arteries, 
and  the  kidneys  has  been  a  fertile  topic  of  discussion.  It  has  been 
explained:  (a)  as  part  of  a  general  process;  (6)  by  the  fact  that 
disease  of  the  kidneys  produced  an  increased  blood-pressure 
reflexly,  this  being  nature's  compensatory  method  of  maintaining 
an  adequate  urinary  output;  (c)  by  assuming  that  the  heart 
lesion  produces  the  renal  lesion  by  means  of  hypostatic  congestion. 
The  occurrence  of  combined  disease  is  very  common. 

1  Friedl.ander:  Arch.  f.  Physiol.,  1881,  p.  168. 

2  Hasenfeld:  Arch.  f.  klin.  Med.,  hx,  210. 

'Scheel:  Ugeskrift  f.  Laegevidenskaben,  Aug.,  1909,  Ixxi. 


Papillary  muscle 


Right  pulmonary 

artery 
Descending  aorta 
Left  bronchus 


Fig.  48. — Sagittal   Section   of  the   Tiiohax.     (See   descriptive  legend   under  Fig,  46.) 

This  figure  illustrate.s:  (1)  the  too  often  insufficiently  appreciated  posterior  position  of 
the  left  auricle,  (2)  the  comparatively  fixed  and  unyielding  structures  by  which  it  is  surrounded: 
the  descending  aorta,  esophagus,  and  spinal  column  behind;  the  left  ventricle  and  diaphragm 
below;  the  left  ventricle  and  right  auricle  in  front.  When  dilatation  of  the  left  auricle  occurs 
it  mu.st  be  upward  mainly.  (.3)  It  is  also  evident  that  direct  pressure  from  the  auricle  upon  the 
aortic  arch  i.s,  on  account  of  the  intervening  structures — the  pulmonary  arteries,  veins  and  the 
left  bronchus — impossible.     (Sec  also  the  Figs.  46  and  47,  and  compare  text,  page  70.) 


152  STUDIES  IN  CARDIAC  PATHOLOGY 

Among  165  autopsies  on  cases  of  cardiac  and  aortic  disease  at  Warsaw,  the 
kidneys  were  normal  in  only  6.  Fifty-four  were  cases  of  mitral,  and  50  of  aortic 
disease.^  In  66  cases  of  chronic  interstitial  nephritis  the  left  ventricle  was  hyper- 
trophied  in  30.5  per  cent.;  normal  or  atrophied  in  58  per  cent.;  both  ventricles 
hypertrophied  in  11.5  per  cent.  In  22  cases  of  arteriosclerosis  the  left  ventricle 
was  hypertrophied  in  27  per  cent.;  right  and  left  ventricles  hypertrophied  in 
9  per  cent.;  normal  in  64  per  cent.  In  25  cases  of  parenchymatous  nephritis 
the  left  ventricle  was  hypertrophied  in  12  per  cent.;  right  and  left  ventricles 
hypertrophied  in  4  per  cent.;  normal  in  84  per  cent. 

Cohnheim's  explanation  of  the  cardiac  hypertrophy  in  nephritis  was  based 
on  mechanical  grounds.  He  attributed  the  rise  of  blood-pressure  to  diminution 
in  the  size  of  the  renal  capillaries  resulting  from  interstitial  nephritis.  But 
Alwen-  was  unable  to  produce  any  considerable  degree  of  hypertension  by  renal 
compression.  Furthermore,  Heinike  and  Paessler's'  progressive  resection  of  the 
kidneys  did  not  prove  that  the  increased  arterial  pressure  was  not  toxic,  rather 
than  mechanical.  Finally,  Jores*  found  less  actual  destruction  of  capillaries 
in  the  red  granular  kidney  than  in  the  atrophic  kidneys  of  late  parenchymatous 
nephritis,  and  in  amyloid  disease,  in  both  of  which  conditions  arterial  hyper- 
tension is  infrequent.  Schur  and  Wiesel,*  on  the  other  hand,  found  a  constantly 
increased  amount  of  adrenalin  in  the  blood  of  nephritics,  and  believe  that  the 
high  blood-pressure  results  from  stimulation  of  the  medullary  portion  of  the 
adrenal  glands.  These  experiments  have,  however,  not  been  corroborated  by 
others.^  Pearce '  has  described  a  nephrotoxic  substance  in  the  blood  of  dogs  in 
which  nephritis  had  been  produced,  which  when  injected  into  normal  dogs  pro- 
duces the  urinary  evidence  of  nephritis.  The  evidence  thus  far,  then,  indicates 
a  chemical  rather  than  a  mechanical  origin  of  the  arterial  hypertension  of 
nephritis. 

Reicher  ^  has  shown  that  in  experimental  nephritis  produced  by  cold,  adren- 
alin is  found  in  increased  amounts  in  the  blood  immediately  succeeding  the  cold 
bath,  indicating  that  perhaps  this  substance  is  the  cause  of  the  hypertension  in 
the  early  stages  of  the  natural  disease. 

Hypertrophy  in  Valvular  Disease. — The  myocardial  changes 
which  follow  experimental  section  of  the  aortic  and  tricuspid 
valves  indicate  a  mechanical  and  not  an  inflammatory  origin. 
The  primary  dilatation  which  follows  the  operation  produces  first 

'Bronowski:  Presse  M6dicale,  1904,  No.  99. 
2  Alwen:  Deut.  Arch.  f.  klin.  Med.,  xcviii,  137. 

^  Heinike  and  Paessler:  Verhandl.  d.  deutsch.  path.  Gesellsch.,  1905,  p.  99. 
^  Jores:  Verhandl.  d.  deutsch.  path.  Gesellsch.,  1908,  p.  187. 
■^  Schur  and  Wiesel:  Verhandl.  d.  deutsch.  path.  Gesellsch.,  1907,  p.  17.5. 
'5  Asohoff  and  Cohn:   Verhandl.  d.  deutsch.  path.  Gesellsch.,  1908,  p.  31.     Goldschmidt : 
Deut.  Arch.  f.  klin.  Med.,  xcix,  186. 

'  Pearce:  Jour.  Med.  Research,  1908,  2. 

"  Reicher:   Berlin,  klin.  Woch.,  1908,  No.  31. 


Fig.  49. — Left  Ventricular  Hypertrohpy. 

A  ca.se  of  aortic  and  mitral  stenosis.  The  aortic  valves  have  unfortunately  been  destroyed 
through  handling.  The  mitral  valve  shows  marked  induration  oj  the  leaflets  and  chordw  tendinem, 
together  with  a  Jew  old  fibrous  vegetations.  The  papillary  muscles  are  hyperlrophied.  (Specimen 
from  the  German  Hospital,  Philadelphia.) 


154  STUDIES   IN    CARDIAC    PATHOLOGY 

an  increase  of  connective  tissue,  later  a  muscular  hypertrophy. 
These  changes  may  occur  independently  of  each  other.  ^  This  is 
opposed  to  the  older  teaching  of  Albrecht,  whose  views  were 
based  upon  a  study  of  human  hearts,  mostly  in  cases  of  nephritis, 
in  which  condition  serositis  and  other  inflammatory^  changes  are 
common.  TangP  has  shown  that  even  in  the  most  emaciated 
animals  hypertrophy  of  the  left  ventricle  will  develop  after  arti- 
ficially produced  valvular  lesions. 

Hypertrophy  is  a  result  of  the  prolonged  overexertion  of  the 
heart  muscle  which  is  required  to  supply  the  demands  of  some 
abnormal  condition  of  the  circulation.  It  is  the  result  of  cardiac 
compensation  under  these  conditions,  not  the  cause  of  it.  The 
experimental  section  of  an  aortic  valve  is  followed  by  dilatation 
of  the  ventricle,  and  almost  equall}^  soon  a  dilatation  of  the  auricle, 
together  with  a  mitral  sj^stolic  murmur.  There  is  no  faltering 
of  the  circulation;  the  animals  are  active  and  playful  and  ap- 
parentlj^  never  suffer  from  edema  or  dyspnea;  all  of  which  facts 
show  that  a  normal  myocardium  is  instantly  able  to  do  an 
enormously  increased  amount  of  work  without  being  prepared 
for  it  by  any  process  of  hypertrophy.  Even  in  long-standing- 
experimental  lesions  there  do  not  seem  to  be  produced  any 
of  those  chronic  myocardial  changes  which  we  find  in  human 
hearts. 

Schnackers^  found  that  even  when  domestic  animals  develop 
endocarditis  by  natural  channels  of  infection,  these  lesions  are 
not  followed  by  myocardial  changes  at  all  comparable  to  those 
which  occur  in  human  beings.  The  Purkinje  fibers,  on  the  other 
hand,  seem  to  be  seriously  damaged. 

Hypertrophied  hearts  of  large  dimensions  are  also  met  with 
as  a  result  of  excessive  beer-drinking  over  prolonged  periods — 
"beer  heart,"  "Munich  heart."  This  lesion  results  not  so  much 
from  any  poisonous  effect  of  the  beer,   but  from   an  increased 

'  Stadler:   Deut.  Arch.  f.  klin.  Med.,  Aug.,  1907,  xci. 

^  Virchow's  Archiv,  cxvi,  432. 

»  Schnackers:  Frankfurter  Zeit.  f.  Path.,  1909,  p.  658. 


Fig.  50. — HypisnTROPHY  and  Dilatation  of  the  Left  Ventricle. 

The  miirnl  valve  .-ihrni-s  inniirroiis  olil  injlammalnry  vegelaliotts,  wilh  more  or  less  deslrucliort 
of  lisHue.  The  left  aunri/lnr  u-nll  in  itUcniKiliil  iiml  its  cavity  enlarged.  (Specimen  from  the 
Episcopal  Hospital,  Pliihi'lilphin.! 


156  STUDIES  IN  CARDIAC  PATHOLOGY 

artificial  plethora  caused  by  the  ingestion  of  excessive  quantities 
of  fluid,  which  in  turn  necessitates  an  increased  systolic  output. 

The  left  ventricle  is  hypertrophied  in  cases  of  aortic  aneurism 
only  if  there  is  an  insufficiency  of  the  aortic  valves. 

"Idiopathic  hypertrophy"  has  been  reported  as  occurring  even 
in  infancy.  Some  of  these  cases  occurred  in  nurslings.  All  sorts 
of  explanations  have  been  offered,  from  Virchow's  suggestion  that 
we  were  dealing  with  a  diffuse  form  of  rhabdomyoma,  to  Michaud's 
belief  that  the  chromaffin  system  is  at  fault. ^  The  majority  of 
the  cases,  however,  occur  in  the  fourth  or  fifth  decade  of  life. 
More  or  less  constant  arterial  hypertension  is  generally  present, 
which  cannot  be  satisfactorily  explained  by  the  urinary  examina- 
tion. Not  infrequently  such  cases  terminate  after  the  manner  of 
nephritics.  The  hypertension  seems  to  be  in  part  the  result  of 
metabolic  toxemia,  and  in  part  the  result  of  adrenal  overactivity, 
and  until  the  relationship  between  these  conditions  and  chronic 
interstitial  nephritis  is  better  understood  we  can  hardly  expect 
definite  knowledge  concerning  this  so-called  "idiopathic  hyper- 
trophy." 

Many  of  the  discordant  reports  which  have  from  time  to  time 
appeared  in  medical  literature  regarding  the  presence  or  absence 
of  hypertrophy  of  certain  heart  chambers  have  been  due  to  inexact 
methods.  The  most  satisfactory,  although  a  time-consuming, 
method  of  determining  this  question  is  known  as  "Mailer's 
method,"  which  consists  of  careful  weighing  of  the  separated 
heart  chambers  after  the  blood-clots,  excess  fat,  etc.,  have 
been  removed.  This  is  much  more  satisfactory  than  measurement, 
since  with  the  latter  procedure  marked  variations  occur  which 
depend  on  whether  the  heart  has  ceased  to  contract  in  systole  or 
in  diastole. 

The  question  as  to  why  a  hypertrophied  heart  fails  in  compensation  has  not 
been  definitely  settled.     Krehl  regards  it  as  due  to  a  progressive  myocarditis. 

'  References  to  this  subject  together  with  a  criticism  of  the  cases  reported  in  the  litera- 
ture will  be  found  in  Hedinger's  article,  Virchow's  Archiv,  vol.  cxxviii,  1904,  and  in  that 
of  Michaud,  Correspondenzbl.  f.  Schweitz.  Aerzte,  1906,  p.  779. 


VUi.    51. Hvi'KRTItOl'HY    AND    DILATATION    OF    THE    LeFT    VeNTRICLE. 

Chronic  miiral  and  aortic  endocardilis.  The  left  ventricular  wall  is  enormously  thickened 
and  the  cavity  enlarged.  The  mitral  valve  shows  extensive  sclerosis.  Many  of  the  chordce  ten- 
dinete  have  ruptured;  the  rest  are  thickened  and  contracted.  Numerous  old  sclerotic  elev- 
ated patches  are  seen  on  the  auricular  .surface  of  the  mitral  leaflets — the  remnants  of  a  former 
endocarditis.  The  pupillary  7nuscles  are  hypcrlrophicd  anil  the  left  iiuricte  is  diluted.  (R])('ci- 
mnn  from  tho  Philadolphia  Hospital.) 


158  STUDIES  IN  CARDIAC  PATHOLOGY 

On  the  other  hand,  the  careful  researches  of  Aschoff  and  Tawara  failed  to  find 
such  changes  sufficiently  constant  to  account  for  the  condition.  So,  too,  the 
studies  of  Lissauer^  fail  to  decide  the  question  as  to  whether  the  cardiac  paralysis 
results  from  a  progressively  increasing  demand  upon  the  heart  muscle,  or  from 
lesions  in  the  nervous  mechanism. 

A  chemical  explanation  of  the  cause  of  myocardial  weakness  has  been  offered 
by  Rzentkowski,  who  found  that  the  myocardium  of  the  left  ventricle  from  cases 
dying  of  prolonged  illness,  but  without  actual  cardiac  disease,  contained  more 
proteid,  fat,  glycogen,  etc.,  and  much  less  sodium  chlorid  than  the  right  ventricle. 
He  has  endeavored  to  explain  heart  failure  by  an  insufficiency  of  these  substances, 
or  by  disturbances  in  their  distribution  or  in  their  utilizability.- 

Bence,  on  the  other  hand,  found  that  neither  hypertrophy  nor  exhaustion  of 
a  heart  chamber  was  associated  with  any  abnormality  in  the  distribution  of 
nitrogen  in  the  heart  muscle,  and,  further,  that  in  normal  and  simple  hj^per- 
trophied  hearts  the  proportion  of  nitrogen  bore  a  constant  relation  to  weight. 
During  exhaustion  the  relation  between  muscular  weight  and  nitrogen  content 
departs  from  the  normal,  inasmuch  as  the  fixed  nitrogen  becomes  proportion- 
ately less.' 

Merkel  *  suggests  that  stasis  in  the  coronary  veins  plays  a  role  in  preventing 
a  removal  of  waste  products,  especially  since  this  blood  is  not  carried  off  by 
collateral  circulations.  Pratt'  failed  to  find  sufficient  fatty  change  to  account 
for  it,  and  Faverges'"  investigations  indicated  that  the  austere  prognosis  in 
fatty  degeneration  was  very  much  overrated.  Aschoff  was  unable  to  find  the 
interstitial  changes  in  either  muscle-,  nerve-,  or  ganglion-cell  which  Daddi  ^  had 
described.  Merkel  and  Jannin*  have  demonstrated  by  means  of  injection  of 
the  coronary  arteries  the  fact  that  in  cases  of  left  ventricular  hypertrophy  there 
is  an  enormous  increase  in  the  vascular  supply  which  is  given  off  from  the  left 
artery,  and,  further,  the  fact  that  the  right  and  left  coronary  arteries  anastomose 
both  as  arterioles  and  as  capillaries,  and  that  anastomotic  branches  from  the 
pericardium  to  the  heart  exist.  In  some  cases,  of  course,  the  hypertrophy  fails 
as  the  result  of  those  changes  which  are  associated  with  advancing  years.  It 
also  fails  in  many  cases  because  the  pathologic  changes  in  other  organs  \vith 
which  it  is  associated  are  progressive  and  have  a  direct  physiologic  as  well  as 
anatomic  relation  to  it.  For  the  present  we  must  conclude  that  the  insufficiency 
of  hypertrophy  rests  upon  a  variable  basis,  and  that  although  some  cases  can  be 
explained  upon  anatomic  grounds,  in  others  we  have  to  assume  a  physico- 
chemical  or  functional  basis.  The  role  of  the  vasomotor  system  is,  as  it  is  in 
infectious  diseases,  more  important  than  is  generallj'  recognized. 

'  Lissauer;   Mtinch.  med.  Woch.,  1909,  No.  36. 

-  Zent.  f.  klin.  Med.,  1910,  Ixx,  337. 

'  Zeit.  f.  klin.  Med.,  Ixvi,  Nos.  .5  and  6. 

'  Merkel:   Mtinch.  med.  Woeh.,  1907,  p.  753. 

*  Pratt:  Quoted  Zentralb.  f.  path.  Anat.,  190.5,  p.  531. 

"  Faverges:  Wien.  klin.  Woch..  1905,  No.  19. 

'  Daddi:  Zentralb.  f.  inn.  Med.,  1904,  p.  119. 

'  Merkel  and  Jannin:  Centralb.  f.  allg.  Path.  u.  path.  Anat.,  1907,  xvii,  876. 


I''iG.  52. — Cardiac  Dilatation. 

The  heart   is   lar^c  ainl    fl:il)by,   its   walls    thinned.      Its  form   k  .somcwlint  (inadrannulur. 
'Photograph  by  Dr.  Alfred  R.  Allen.) 


160  STUDIES  IN  CARDIAC  PATHOLOGY 

In  a  study  of  the  cause  of  compensatory  failure  in  34  cases  of  hj'pertrophy, 
Schltiter'  found  fatty  degeneration  of  the  muscle-fibers  relatively  frequently, 
together  with  enlargement  and  chstortion  of  the  nuclei.  Connective-tissue  or 
round-cell  infiltration  was  less  common  and  more  localized.  He  behaves  that 
these  manifestations  are  not  the  anatomic  expression  of  heart  weakness,  but  the 
results  of  insufficient  cardiac  activity — slowed  circulation  and  lymphatic  stasis. 
Insufficiency  of  the  hypertrophied  ventricle  is  the  result  of  inadequate  reserve 
power,  which  he  attributes  rather  to  chminished  excitabihty  than  to  actual 
muscular  disease. 

'  R.  Schliiter:   Die  Erlahmung  des  hypertrophieten  Herzmuskels,  Vienna,  1906. 

Fig.  53. — Hypertrophy  and  Dilatation  of  the  Heart. 

W.  B.  (Philadelphia  Hcspital.  November  28,  1901.  xiii:  103.  Patliologist:  Dr. 
Prince.) 

Pathologic  Diagnosis:  Myocarditis;  bilateral  pleural  effusion;  hypertrophy  and  dila- 
tation of  the  heart;  mitral  insufficiency;  aortic  stenosis;  advanced  arteriosclerosis;  edema  of 
the  lungs;  acute  nephritis. 

Pericardium:   Contains  100  c.c.  of  fluid. 

Heart:  Weighs  760  gm.  The  muscle  is  pale,  the  mills  fn'uhlr.  Tlir  hf I  rentricle  averages 
1.5  cm.  in  thickness.  The  aortic  valves  are  incompetent.  I  In  n-chiixi/urLi  ikiI  a  ml  Indurated.  The 
mitral  ring  admits  five  fingers;  its  valve  leaflets  are  sliyhllij  llilcl.-i  ncil.  The  mnia  is  practically 
one  mass  of  atheromatous  plates,  with  excavations.  The  left  ventricular  cavity  shows  many  cal- 
careous plates,  and  is  about  twice  the  normal  size. 


X.  CARDIAC  DILATATION 

Pathogenesis. — By  dilatation  of  the  heart  we  mean  an  increase 
in  the  size  of  its  chambers,  which  results  from  stretching  of  its 
muscular  walls.  Such  a  condition  may  occur  acutely  under  sud- 
den, prolonged,  or  excessive  strain,  especially  in  subjects  out  of 
training,  or  as  the  result  of  toxic  processes,  such  as  diphtheria, 
typhoid  fever,  pneumonia,  also  as  the  result  of  prolonged  nervous 
strain  and  sudden  mental  or  moral  shock.  The  emotional  stress 
acts  on  the  vasomotor  nerves,  the  arterial  spasm  inducing  a  hyper- 
tension which  reacts  on  the  myocardium.  It  has  also  been  sug- 
gested that  the  moral  shock  has  further  a  direct  action  on  the 
centers  regulating  the  innervation  of  the  heart.  Such  cases  were 
observed  among  the  Jews  during  the  massacres  in  Odessa.  ^  Chronic 
dilatation  of  the  heart  is  generally  associated  with  or  a  sequel 
of  hypertrophy.  It  is  usually  due  to  two  factors:  inadequate 
nutrition  and.  increased  endocardial  pressure,  such  as  occurs  in 
the  gradual  occlusion  of  sclerotic  coronary  arteries,  together  with 
valvular  disease  and  an  increased  demand  for  hypertrophy. 
Increased  endocardial  pressure  may  result  not  only  from  dim- 
inished outflow,  but  also  from  increased  inflow — from  a  rise  of 
venous  pressure. 

When  extra  work  is  suddenlj'  required  of  tlie  ventricle,  as,  for  instance,  if 
the  aorta  is  clamped,  there  first  results  a  dilatation  of  the  chamber  associated 
with  a  diminution  of  the  systolic  output;  following  this  in  healthy  hearts  there 
occurs  as  the  result  of  increased  tonicity  an  increase  of  the  systohc  output,  so 
that  the  ventricle  again  empties  itself  properly.  But  if  the  heart  is  unable  to 
meet  the  emergency,  or  the  obstructive  force  is  too  great,  dilatation  ensues 
(0.  Frank,  Hirschf elder). 

From  what  has  been  said  it  will  be  readily  understood  that,  as 
seen  at  autopsy,  dilatation  of  the  heart  is  generally  associated 

'  Cheinisse:  Semaine  Medic,  1907,  xxvii,  No.  9. 
162 


I'u;.  .54. — Ax  ExTKK.MK  Grade  of  .Sclerosis  and  Calcification  of  the  Aortic  Valves 

AND    OF   THE    AoRTA   ItSELF. 

The  valves  are  shrunken,  thickened,  stiffened,  and  show  calcareous  change;  the  aorta  is 
dilated  and  consists  of  great  masses  of  calcareous  infiltration,  for  the  purpose  of  showing 
which  the  vessel  has  been  everted.  The  mitral  valve  is  sclerotic.  The  aortic  valves  are  cal- 
cified, the  ventricular  endocardium  is  thickened,  and  the  left  ventricle  is  hypertrophied  and 
dilated.  The  aorta  .shows  as  saccular  aneurismal  dilatation.  (Specimen  from  the  Philadel- 
phia HoHpital.) 


164  STUDIES  IN  CARDIAC  PATHOLOGY 

with  more  or  less  hypertrophy,  in  those  cases  in  which  the  causa- 
tive factors  have  been  of  prolonged  duration. 

Simple  dilatation  without  a  preceding  hypertrophy  may  result 
from  the  toxemia  of  infectious  disease,  especially  diphtheria,  from 
metabohc  poison,  as  in  uremia,  from  lack  of  nutrition  or  the 
ingestion  of  poison,  or  from  sudden  exertion,  and  apparently  at 
times  from  psychic  shock.  ^ 

There  can  hardly  be  a  doubt  that  toxins  play  an  extrem^ely 
important  role  in  the  production  of  dilatation.  The  microscopic 
examinations  by  Tawara  on  the  hearts  of  patients  dead  of  cardiac 
failure  in  a  large  number  of  cases  showed  no  changes  which  could 
account  for  death.  The  sudden  death  in  infections  such  as 
diphtheria  is  an  example.  In  diphtheria  this  sudden  death  is 
usually  attributed  to  toxic  action  on  the  vagus,  inasmuch  as  it  is 
often  associated  with  unexplained  and  sudden  vomiting,  and  since 
post-diphtheritic  paralyses  are  well  known.  So,  too,  the  question 
has  been  brought  up  whether  diphtheria  does  not  more  or  less 
often  irreparably  damage  the  heart  so  that  sudden  death  may 
occur  months,  or  even  years,  after  the  original  infection. 

Morbid  Anatomy. — The  heart,  in  addition  to  being  enlarged, 
is  relaxed,  flabby,  and  distended  with  blood.  Dilatation  generally 
affects  chiefly  the  right  side.  The  auriculo-ventricular  orifices 
are  enlarged,  the  septa  may  bulge  toward  the  less  affected  side, 
while  chronic  mj^ocardial  changes  of  a  fatty  or  fibroid  nature  are 
more  or  less  evident.     (See  Fig.  52.) 

It  is  doubtful  if  all  cases  of  cardiac  dilatation  could  be  ex- 
plained on  an  anatomic  basis,  even  if  our  methods  of  examination 

'  Two  cases  reported  by  Marmorstein,  Wien.  med.  Woch.,  Aug.  4,  1906.  Starck:  Mlinch. 
med.  Woch.,  1905,  lii,  No.  7. 

Fig.  .5.5. — Calcification  of  the  Aorta. 

Specimen  showing  the  left  ventricular  cavity.  The  .aortic  valves  are  thickened,  slightly 
retracted,  and  contain  calcareous  deposits.  The  aorta  is  greatly  thickened  and  its  entire  sur- 
face is  covered  with  white  and  dark  yellow,  roughened  and  projecting  calcareous  plates. 
(Yellow  being  a  relatively  non-actinic  color,  these  plates  appear  as  black  and  brown  in  the 
reproduction.)  The  mitral  valve  is  moderately  thickened.  (vSpecimen  from  the  Philadelphia 
Hospital.) 


166  STUDIES    IN    CARDIAC    PATHOLOGY 

were  more  searching  and  exact.  Dilatation  is  essentially  the  result 
of  diminished  muscular  tone,  and  while  doubtless  many  cases 
can  be  explained  by  structural  microscopic  changes  in  the  muscle- 
fibers  or  nerves,  yet  we  know  that  muscular  tone  varies  greatly 
within  functional  limits. 

Clinical  Considerations. — There  has  been  much  discussion  and 
investigation  regarding  the  existence  of  a  functional  cardiac 
dilatation.  It  was  at  one  time  taught  that  the  so-called  "second 
wind"  of  the  well-trained  athlete  depended  upon  the  appearance 
of  a  physiologic  dilatation  by  virtue  of  which  the  heart  was  enabled 
to  handle  more  blood.  The  investigations  of  Dietlen,  Moritz, 
De  la  Camp,^  Raab,''  and  others  indicate  that  such  is  not  the  case. 
On  the  contrary,  the  normal  heart  becomes  smaller  during  severe 
exertion,  and  when  dilatation  occurs,  we  are  in  all  probability 
dealing  with  an  organ  whose  reserve  power  is  not  up  to  par. 

We  must  also  bear  in  mind  that  the  normal  heart  is  smaller  in  the  erect 
than  in  the  recumbent  postures,  due  to  the  fact  that  in  the  former  a  larger  amount 
of  blood  is  pent  up  in  the  vessels  below  the  heart  by  the  action  of  gravity.^ 
It  is  also  possible  that,  pressure-tension  of  the  pericardium  being  greater  in  the 
standing  position,  a  greater  pressure  is  exerted  not  only  on  the  heart  itself,  but 
also  upon  the  venae  cavae,  both  of  which  would  tend  to  lessen  the  blood-content 
of  the  heart,  as  would  also  lowering  of  blood-pressure  and  increase  of  pulse-rate. 

Dilatation  sometimes  results  from  pure  fatigue  of  the  muscle, 
no  structural  changes  being  demonstrable.  Dilatation  by  bulging 
of  the  ventricle  drags  on  the  papillary  muscles  and  makes  it  more 
difficult  for  the  auriculo-ventricular  valves  to  close,  thus  producing 
valvular  incompetency^ 

Although  the  consideration  of  myocarditis  properly  belongs  to 
a  work  which  concerns  itself  with  microscopic  pathology,  yet  the 
subject  is  so  intimately  associated  with  the  conditions  which  we 
have  discussed  that  a  brief  allusion  to  certain  phases  seems  war- 
ranted. 

Acute  myocarditis  may  occur  as  a  result  of  infectious  processes 

'  De  la  Camp:   Zeit.  f.  klin.  Med.,  vol.  li. 
"  Raab:   Milnch.  med.  Woch.,  1909,  No.  11. 
^Dietlen:   Habilitationsschrifft,  1909. 


Fk;.  56. — CALCiFirATioN  of  the  Aorta. 

The  entire  aorta  is  one  hard,  brittle,  rough,  thickened,  calcareous  mass,  which  fractures 
with  an  audible  snap  when  the  vessel  is  flexed.  The  aortic  valves  share  in  this  process  of 
calcification.  The  wall  of  the  left  ventricle  is  greatly  thickened.  The  pericardium  is  thick- 
ened and  the  subpericardial  fat  increased  in  amount.  (Specimen  from  the  German  Hospital, 
Philadelphia.) 


168  STUDIES  IN  CARDIAC  PATHOLOGY 

either  as  the  result  of  micro-organismal  or  toxic  action.  It  is 
met  with  more  especially  in  diphtheria,  typhoid  and  typhus 
fevers,  rheumatic  fever,  scarlatina,  and  influenza.  Embolic  and 
thrombotic  affections  of  the  coronary  vessels,  and  septic  processes, 
may  also  be  causative  factors.  The  toxemia  of  pregnancy, 
especially  when  eclampsia  has  occurred,  often  causes  myocardial 
degeneration. 

Chronic  myocarditis  is  often  the  result  of  poor  cardiac  nutrition, 
which,  in  turn,  means  that  the  coronary  circulation  has  in  some 
way  been  rendered  inadequate.  Thus,  sclerosis  of  these  vessels 
leads  to  fibroid  or  fatty  changes  according  to  the  amount  of  vas- 
cular damage.  Again,  valvular  lesions,  especially  aortic  obstruc- 
tion, lead  to  myocarditis,  because  with  an  increased  demand  for 
cardiac  work  there  is  a  relative  diminution  of  blood-supply. 
Coronary  sclerosis  may  arise  from  conditions  similar  to  those 
which  cause  arteriosclerosis  elsewhere.  We  must  bear  in  mind, 
however,  that  the  mouths  of  these  vessels,  arising  as  they  do  from 
the  aorta  in  close  proximity  to  the  heart,  are  often  seriously  con- 
stricted at  their  point  of  origin  as  the  result  of  disease  of  the  aorta, 
without  there  being  anj^  marked  pathologic  changes  in  their  later 
course.  It  is  in  this  respect  especiallj;'  that  syphilitic  aortitis 
plaj^s  so  important  a  role,  producing,  as  it  does  with  great  fre- 
quency, aortic  aneurism,  aortic  insufficiency,  and  myocarditis. 
That  this  statement  does  not  invariably  apply,  however,  is  indi- 
cated by  the  experimental  work  of  Fleisher  and  Loeb,  who  found 
that  adrenalin  injections,  when  combined  with  certain  other 
substances,  such  as  spartein  sulfate  and  caffein  sodium  benzoate, 
produce  both  macroscopic  and  microscopic  myocardial  changes.^ 

The  direct  cause  of  these  lesions  seems  to  be  a  mechanical  one.  "The 
typical  seat  of  the  lesion  at  the  base  of  the  left  ventricle,  where  the  greatest 
strain  is  exerted,  favors  this  theory.  Furthermore,  analogous  conditions  have 
been  shown  to  occur  in  striated  muscle  in  conditions  of  overexertion.     The  fact 

1  Fleisher  and  Loeb's  article,  Arch.  Int.  Med.,  Feb.,  1909,  contains  also  a  resumd  of  the 
literature  concerning  experimental  myocarditis.  See  also  a  second  article  by  the  same  authors, 
Arch.  Int.  Med.,  Oct.  15,  1910. 


Fig.  57. — Sclerotic  .\nd  Calcified  Coronary  Arteries. 

Specimen  from  the  Museum  of  the  University  of  Pennsylvania,  showing  the  root  of  the 
aorta  and  the  coronary  arteries,  the  myocardium  being  removed  by  dissection.  The  vessels 
are  greatly  thickened,  and  consi.st  of  masses  of  calcareous  nodules  and  plates. 


170  STUDIES  IN  CARDIAC  PATHOLOGY 

that  the  injection  of  spartein  and  aclrenahn  into  dogs,  whose  hearts  are  relatively 
stronger  than  those  of  rabbits,  does  not  cause  the  appearance  of  myocardial 
lesions,  adds  further  support  to  this  theory.  These  lesions  are  in  all  probability 
not  clue  to  lack  of  nutrition  of  the  muscle-fibers  as  a  result  of  contraction  of  the 
coronary  vessels,  inasmuch  as  it  has  been  shown  that  adrenalin  does  not  cause  a 
contraction  of  these  vessels." 

Even  small  doses  of  adrenalin  in  the  rabbit  produce  well-marked  myocardial 
changes,  although  these  lesions  show  a  tendency  to  heal.  Pearce'  has  shown 
that  large  quantities  of  this  substance  injected  into  animals  may  produce  sudden 
death  from  acute  dilatation  or  from  insidious  myocardial  changes  which  occur 
independently  of  coronary  sclerosis. 

Bjorksten  succeeded  in  producing  myocardial  changes  in  animals  by  the 
injection  of  micro-organisms  (bacillus  coli,  pneumococcus,  typhoid  bacillus, 
staphylococcus),  and  also  of  their  toxins.-  Similar  results  were  obtained  by 
Arloing  and  De  Lagoanere  with  streptococci  and  staphylococci.'' 

Rheumatic  myocarditis  is  etiologically  one  of  the  most  im- 
portant varieties.  It  accompanies  most  cases  of  rheumatic  endo- 
carditis, and  it  is  to  this  pathologic  process  that  many  cases  of 
cardiac  hypertrophy  and  chronic  myocarditis  owe  their  origin. 
Macroscopically  rheumatic  myocarditis  shows  httle  that  is  char- 
acteristic. Microscopically  an  inflammatory  tissue  proliferation 
which  manifests  itself  as  small  interstitial  nodules  is  noted.  This 
process  spreads  to  the  neighboring  muscle-fibers  and  produces 
degeneration  in  them.*  The  hypertrophy  and  dilatation  affects 
both  ventricles,  and  is  often  considerable,  more  so  than  the 
microscopic  changes  seem  to  account  for.  Ventricular  hyper- 
trophy and  dilatation  are  evidently  the  result  of  toxic  action. 
Death  in  the  rheumatic  carditis  of  childhood  is  generally  directly 
due  to  the  myocardial  lesions.'^  The  nodules  above  referred  to 
are  by  some  considered  characteristic  of  rheumatic  infection,  but 
they  have  also  been  described  as  occurring  in  chronic  nephritis 
and  in  non-rheumatic  infections.  Rheumatic  myocarditis  tends 
to  be  progressive,  a  progression  which  is  often  considerably  en- 
hanced by  subsequent  reinfections. 

'  Pearce:  Albany  Med.  Annals,  Jan.,  1907,  p.  42. 

-  Bjorksten:   Arbeit,  path.-anat.  Institut  Helsingfori?,  1908. 

■'  Arloing  and  De  Lagoanere:  These  de  Lyon,  190S. 

'  Geipel:   Deut.  Arch.  f.  khn.  Med.,  Ixxxv,  p.  75. 

=  Coombs:  Quart.  Jour.  Med.,  Oct.,  1908,  p.  26. 


Fia.  58. — Cardiac  Aneurism. 

'rhc  lower  part  of  the  loft  ventricle  shows  a  marked  protuberance  both  to  the  right  and  to 
the  left  of  the  incision.  On  the  external  surface  of  this  bulging  area  the  pericardium  is  densely 
adherent.  The  ventricular  wall  at  this  point  is  thinned  and  the  muscle  appears  dark  and  softer 
than  elsewhere.  The  interior  of  the  sac  communicates  directly  with  the  left  ventricular  cavity. 
At  the  lowermost  end  of  the  incision,  part  of  a  dark  blood-clot  is  seen  which  extends  into,  and 
to  a  certain  extent  fills,  the  sac.  The  left  ventricle  is  hypcrtrophicd  and  dilated.  The  aorta 
shows  .slight  arteriosclerotic  change,     fSpecimen  from  the  Philadelphia  Hospital.) 


172  STUDIES    IN    CARDIAC    PATHOLOGY 


Fig.  59. — Aneurism  of  the  He.\rt. 

J.  N.,  white,  male,  aged  seventy-seven  years.  (Pennsylvania  Hospital.  Autopsy  No. 
-125.     Pathologist:    Dr.  Longcope.) 

Clinical  Notes:  Admitted  nine  days  ago,  having  been  ill  for  two  or  three  weeks,  with 
cough  and  chilliness.  In  delirium  he  had  wandered  from  his  bed,  to  which  he  was  returned 
only  after  a  tussle.     He  died  suddenly  two  hours  later. 

Physical  Examination:  No  heart  murmurs.  First  sound  faint.  Action  of  heart 
irregular. 

Pathologic  Diagnosis:  Aneurism  of  the  he%rl,  with  rupture  ifito  the  -pericardium. 
Occlusion  of  the  descending  branch  of  the  left  coronary  artery.  General  arteriosclerosis.  Chronic 
diffuse  nephritis. 

Pericardium:  Is  filled  with  blood. 

Heart:  Is  much  enlarged.  The  epicardium  is  filled  with  fat,  which  measures  0.5  cm.  in 
some  places.  The  organ  has  a  peculiar  shape,  due  to  buljing  of  the  left  ventricle,  so  that  the  heart 
from  apex  to  base  is  elongated.  In  the  bulging  tip  of  the  left  ventricle  there  is  a  rupture  4  cm. 
in  length  and  2  cm.  in  width.  The  surface  of  the  heart  about  the  tear  is  mottled  deep  red  and 
brownish-gray  in  color.  On  opening  the  heart  the  right  ventricle  is  normal,  as  are  also  the 
tricuspid  and  pulmonary  valves.  The  left  auricle  is  thickened  but  not  dilated.  The  mitral 
leaflets  are  moderately  thin  and  delicate.  The  tip  of  the  left  ventricle  shows  a  tear  corresponding 
in  position  to  that  described  externally.  It  is  6  cm.  in  diameter.  The  heart  muscle,  which  is 
fairly  firm  and  yellowish-brown  in  color  (near  the  base  of  the  left  ventricle  measuring  2  cm.), 
gradually  thins  out  until  the  deepest  portion  of  the  aneurismal  sac  is  reached,  where  scarcely 
any  muscle-fibers  can  be  found.  At  the  beginning  of  the  sac  the  heart  muscle  is  pale  brown 
and  soft.  The  sac  is  almost  entirely  filled  with  soft  blood-clot,  which  shows  very  beautifully  "the 
lines  of  Zahn."  The  clot  is  attached  to  the  wall  of  the  heart,  and  measures  11  cm.  in  thickness;  it 
Jills  the  sac  except  in  the  lower  portion,  in  which  the  tear  occurred.  The  aortic  valves  are  somewhat 
retracted,  thickened,  and  calcified,  about  the  sinus  of  Valsalva.  The  descending  branch  of  the 
left  coronary  artery  becomes  very  much  narrowed  about  3  cm.  from  its  origin,  and  as  it  reaches 
the  region  of  the  dilatation,  is  completely  calcified  and  practically  occluded.  The  circumflex 
branch  and  the  right  coronary  artery  are  patent,  but  their  walls  are  absolutely  stiff  and  cal- 
careous. The  aorta  shows  moderate  arteriosclerosis  associated  with  large  areas  of  ulceration 
and  atheromatous  ulcers. 

Microscopic  Examination:  The  pericardium  contains  a  good  deal  of  fat,  but  is  normal. 
The  heart  muscle  is  to  a  large  extent  degenerated.  Certain  areas  are  composed  of  pinkish 
granular  material,  mixed  with  the  remains  of  muscle-fibers,  and  some  young  connective -tissue 
cells.  About  the  margin  of  these  areas  the  muscle-fibers  are  swollen  or  atrophied,  filled  with  small 
granules,  and  destitute  of  cross-strije.  The  nuclei  often  do  not  stain.  Between  the  muscle- 
fibers  there  is  either  connective  tissue  or  fat.  In  some  places  isolated  masses  of  muscle-fibers 
are  seen,  which  still  retain  their  structure,  but  are  entirely  necrotic.  The  cells  are  filled  with  a 
golden-brown  pigment  in  the  degenerated  areas.  A  few  polynuclear  leukocytes  are  found. 
The  thickness  of  the  muscular  wall  of  the  heart  measures  in  some  sections  only  1  mm.  Thrombi 
composed  of  erythrocytes,  leukocytes,  and  fibrin,  all  of  which  take  a  rather  definits  eosin 
stain,  are  attached  to  the  endocardial  surface  in  some  sections.  There  is  no  definite  organiza- 
tion, but  the  clot  is  so  clearly  welded  into  the  muscular  wall  that  it  is  impossible  to  determine 
where  the  one  ends  and  the  other  begins.  The  intima  of  some  of  the  small  arteries  is  so  much 
thickened  that  the  lumen  in  some  places  is  almost  occluded. 

Diagnosis:   Myomalacia;   chronic  interstitial  myositis;  thrombosis. 


Fk;    59. 


174  STUDIES    IN    CARDIAC    PATHOLOGY 

The  whole  subject  of  chronic  myocarditis  is  still  far  from 
satisfactorily  understood.  There  have  been  great  discrepancies 
of  results  among  different  observers,  and  hence  diversities  of 
opinion. 

Mj^ocarditis  has  been  attributed  to  a  great  number  of  other 
factors,  such  as  a  strenuous  life,  physical  toil  and  hardship,  chronic 
infections,  and  intoxications — metabolic,  alcoholic,  nicotinic,  etc.; 
but  it  is  very  evident  that  the  majority  of  these  factors  are  of 
etiologic  importance  in  exact  proportion  to  their  tendency  to 
produce  vascular  damage. 

Myocardial  changes  have  also  been  produced  bj^  high  temperatures,  by  the 
injection  of  staphylococcus  pyogenes  aureus,  diphtheria  bacillus  and  toxin,  strep- 
tococcus, adrenalin,  and  ligation  of  the  branches  of  the  coronary  arteries. 

Of  all  infectious  diseases,  diphtheria  is  most  commonly  accompanied  by 
cardiac  dilatation,  scarlatina  being  next  in  frequency.  In  the  majority  there 
is  a  gradual  return  to  the  normal.  In  rheumatic  fever  8  out  of  18  showed  dilata- 
tion; 7  of  these  patients  also  had  endocarditis.  Three  with  endocarditis  showed 
no  dilatation.  None  of  these  cases  returned  to  a  normal  size  (for  bochly  weight). 
In  typhoid  fever  the  return  to  normal  was  variable.  Five  cases  of  pneumonia 
out  of  11  had  dilatation  which  appeared  chiefly  at  the  time  of  the  crisis.' 

The  depressing  effect  of  the  diphtheria  toxin  upon  the  heart  has  long  been 
recognized,  and  has  been  experimentally  demonstrated.-  According  to  Gossage,''' 
the  diphtheria  toxin  depresses  contractility,  the  rheumatic  toxin  tonicity,  hence 
the  greater  frequency  of  death  as  a  result  of  the  former,  and  dilatation  as  that 
of  the  latter. 

In  diphtheria  the  myocardial  complications  increase  with  age:  14.3  per 
cent,  in  children  under  two  years;  88.5  per  cent,  between  eleven  and  fifteen 
years.     Cardiac  dilatation  occurred  in  29  out  of  40  cases.'' 

Influenza,  although  occasionally  causing  endocarditis  or  myocarditis,  gen- 
erally manifests  its  cardiac  effect  by  making  some  already  existing  lesion  worse. ^ 

Acute  syphilitic  myocarditis  as  a  secondary  manifestation  has  been  described 
by  Jesionek. 

Suppurative  myocarditis  includes  two  distinct  types:  (1)  Puru- 
lent infiltration  of  the  heart  muscle,  generally  secondary  to  such  con- 
ditions as  infectious  endocarditis,  pericarditis,  cardiac  thrombosis, 

'  Dietlen  (orthodiagraphic  studies):  Munch,  med.  Woch.,  1908,  p.  2077. 

2  Chevalier  and  Clerc:  Soc.  Biolog.,  June  26,  1909. 

'  Gossage:  Lancet,  Aug.  21,  1909. 

'  Foerster:   Deut.  Arch.  f.  klin.  Med.,  1905,  No.  13. 

'^  Ruheman:   Beriin.  klin.  Woch.,  1910,  p.  201. 


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Fiii.  GO. — CAHDiAf  Thiiombosis. 

A  large  rounded  thrombus  about  the  size  of  a  large  walnut  is  attached  to  the  auricular 
surface  of  the  mitral  valve.  The  valvular  leaflets  themselves  are  sclerosed  and  indurated. 
Another  and  much  larger  thrombus  is  seen  occupying  the  lower  and  anterior  surface  of  the  left 
ventricle.  This  has  undergone  partial  organization  and  is  firmly  attached  to  columna;  carneie 
and  the  ventricular  r^ndocardium,  and  very  materially  reduces  the  size  of  the  cavity. 


176  STUDIES  IN  CARDIAC  PATHOLOGY 

septic  myocardial  infarction,  as  in  pyemia;  (2)  acute  interstitial 
myocarditis,  such  as  may  occur  in  scarlatina,  diphtheria,  etc. 
Beck  and  Stokes  ^  were  able  to  find  only  one  true  case  of  the 
last-named  type  recorded,  although  thej^  collected  a  number  of 
cases  of  circumscribed  abscess  formation.  Suppurative  myo- 
carditis generally  results  from  septic  thrombosis,  and  the  abscesses 
resulting  may  vary  in  size  from  a  pinhead  to  several  centimeters 
in  diameter.  Among  the  9,940  autopsies  studied  by  the  author 
there  were  6  cases  of  acute  suppurative  myocarditis. 

Clinical  Considerations. — While  it  is  doubtless  true  that  the 
myocardium  plays  a  role  in  all  forms  of  heart  disease  the  im- 
portance of  which  it  is  difficult  to  overestimate,  yet  the  term 
"myocarditis"  is  often  vaguely  applied,  and  such  a  diagnosis 
made  without  ample  justification.  Thus,  in  acute  diseases  death 
is  often  attributed  to  myocarditis  when  it  is  really  the  result  of 
toxic  vasomotor  paralysis.  In  these  cases  blood-pressure,  both 
systolic  and  diastolic,  will  be  found  unduly  low,  and  careful 
microscopic  examination  of  the  heart  may  show  no  structural 
alterations  meriting  the  appellation  of  myocarditis.  Surgical 
shock,  too,  is  now  known  to  be  a  vasomotor  paralysis,  and  not 
to  be  a  result  of  heart  weakness.  Sweet  has  suggested  that  it 
may  be  the  result  of  an  acute  adrenal  insufficiency.  A  clinical 
diagnosis  of  myocarditis  is  generally  based  upon  evidences  of 
cardiac  insufficiency^  the  symptoms  of  which  may  be  produced 
by  a  host  of  extracardiac  and  intracardiac  causes,  associated  with 
which  ver}^  little  myocardial  degeneration  may  be  demonstrable 
at  autopsy.  On  the  other  hand,  cases  with  well-marked  lesions 
often  exhibit  disproportionately  few  symptoms.  Cabot  found  a 
myocarditis  correctly  recognized  in  22  per  cent.,  overlooked ,  in 
26  per  cent.,  and  diagnosticated  when  not  present  in  52  per  cent, 
of  the  cases  studied  by  him.  We  must  bear  in  mind,  however, 
that  very  small  lesions  localized  to  important  areas,  such  as  the 
sinus  node,   the  auriculo-ventricular  node  or  bundle,   etc.,  may 

'  Beck  and  Stokes:  Jour.  Am.  i\Ied.  Assoc.,  1910,  p.  1065. 


In;.  01. — CAiii)[.\r  A.\i;i;ris,m  a.vd  Tiuiombosis. 
A  larce  o'/ati;  llirombus  i.s  .s.ion  in  tho  lower  part,  of  the  left  ventricle,  the  walls  of  which  are 
visibly  thinncfl  and  stretchetl  below  and  behind  the  thrombus.     The  endocardium  of  the 
vonlriclo  in  thickened  anrl  riparnic,  the  aorta  xhow.s  slifrhl  artcrio.sclorotic  chango,  in  part  in- 
volving the  mouth  of  thf  cdronary  artery. 


178  STUDIES  IN  CARDIAC  PATHOLOGY 


Fig.  62. — Mural  Thrombosis. 

Pathologic  Diagnosis:  Mural  cardiac  thrombosis.  Dilatation  of  the  heart,  chronic 
myocarditis,  bronchopneumonia. 

Pathologic  Notes:  Pericardium:  The  pericardium  contains  approximately  20  c.c.  of 
clear  yellow  straw-colored  fluid.  The  visceral  surface  is  smooth  and  glistening,  with  injected 
vessels.  Its  visceral  surface  contains  a  large,  smooth,  opaque,  white  patch  measuring  3x2  cm. 
This  patch  is  apparently  on  the  external  surface  of  the  middle  portion  of  the  right  ventricle. 
There  are  a  few  scattered  areas  similar  to  the  above  on  the  external  surface  of  the  right  heart. 
The  superior  portion  of  the  exterior  surface  of  the  right  auricle  contains  a  few  yellowish-white 
■  spots,  pinhead  size.     There  is  a  larger  yellowish-white  patch,  5  mm.  in  diameter. 

Heart:  The  heart  weighs  530  grams.  The  heart's  flesh  is  quite  firm  in  consistency  and  is 
of  a  dark  red  color  streaked,  in  areas,  with  spots  of  a  lighter  red.  Both  the  right  and  left  heart 
are  markedly  dilated.  The  right  ventricular  walls  measures  5  mm.  in  thickness.  The  papil- 
lary muscles  are  of  a  pale  reddish-gray  color.  Clinging  to  portions  of  the  right  ventricular 
wall,  especially  toward  its  tricuspid  portion,  are  masses  of  a  quite  firm  reddish  material  spotted 
with  areas  of  yellow.  These  masses  are  quite  well  attached  to  the  muscular  wall,  and  for  the 
most  part  lie  between  the  papillary  muscles.  The  right  auricle  is  completely  thrombosed 
by  the  masses  of  what  appear  to  be  organized  blood-clots.  The  muscle  of  the  right  ven- 
tricular wall,  especially,  shows  on  its  under  surface  very  many  reddish-yellow  patches  with 
small  strands  of  reddish  tissue  coursing  between  them,  which  gives  to  the  surface  a  mottled 
appearance.  At  the  base  of  many  of  the  papillary  muscles  small  whitish  patches  are  seen. 
The  tricuspid  valve  is  well  formed  and  normal  in  all  respects.  The  pulmonary  valve  shows  no 
apparent  pathologic  change,  nor  do  the  pulmonary  vessels.  The  endocardium  of  the  right 
side  seems  to  be  intact.  The  lefl  rntiriciilar  cavity  is  dilated,  measuring  at  its  middle  transverse 
portion  10.5  cm.  The  muscuhir  imll  i-nrirf;  in  thickness;  thus,  at  the  apex  it  is  but  1  cm.  in  thick- 
ness, while  toward  the  valvular  end  it  measures  1.7  cm.  in  thickness.  Attached  to  its  walls  are 
masses  oj  an  organized  tissue  of  a  reddish-gray  appearance,  streaked  with  coarse  strands  of  a 
definite  yellow-while.  These  masses  cling  to  nearly  all  portions  of  the  left  ventricular  wall,  measur- 
ing from  0.5  to  2.5  cm.  in  diameter,  and  do  not  appear  to  cling  to  the  endocardium  at 
any  point.  The  condition  of  the  heart  muscle,  at  its  .junction  with  these  clots,  has  a  most 
peculiar  appearance.  Where  the  clots  nice!  the  true  muscular  wall  there  appears  to  be  a 
dcHiiitc  yellow  line,  in  many  portions  shouinii  ilisiiiici  (Iciiiarkation.  These  clots  interweave 
among  the  papillary  muscles,  are  quiti'  finu  in  coiisislcncy,  and  show  definite  evidences  of  well 
organized  tissue.  The  mitral  valve  is  normal.  The  left  auricle  contains  the  same  kind  of 
thrombi  as  does  the  ventricle.  The  aortic  ring  measures  6  cm.  The  aortic  valves  are  well 
formed  and  are  normal  in  all  respects.  There  is  no  evidence  of  any  sclerosis  of  the  larger 
vessels.  The  coronary  arteries  are  patent;  their  walls  are  smooth  and  no  sclerosis  can  be 
found.     (Pennsylvania  Hospital,  No.  1060.) 


Fig.  62^ 


180  STUDIES  IN  CARDIAC  PATHOLOGY 

apparently  be  responsible  for  serious  damage  when  the  rest  of  the 
myocardium  is  comparative!}'  healthy;  and  that  disease  of  these 
structures  is  generally  undemonstrable  during  a  routine  autopsy. 
It  is  to  be  hoped  tliat  the  careful  routine  examination  of  these 
areas  in  large  series  of  cases  will  throw  much  light  upon  the  at 
present  unsatisfactory  status  of  "myocarditis." 

CORONARY  ARTERIOSCLEROSIS 

The  nutritional  suppl}',  and  hence  the  functional  integrity^,  of 
the  whole  heart  depends  very  largely  upon  the  condition  of  the 
coronary  arteries.  As  long  as  the  blood-supply  is  adequate  the 
heart  can  cope  with  the  most  surprising  mechanical  odds.  It  is 
not  surprising,  therefore,  that  sclerosis  of  the  coronary  arteries 
should  be  the  most  serious  form  of  heart  disease. 

As  a  general  rule,  gradual  narrowing  of  a  coronary  artery  is 
followed  by  fibroid  or  fatt_y  change  in  the  mj^ocardium,  whereas 
sudden  occlusion,  as  may  occur  from  embolism  or  thrombosis, 
produces  an  area  of  softening  somewhat  smaller  than  the  anatomic 
area  supplied  by  the  vessel.     (See  Section  IX.) 

Although  the  earlier  teaching,  that  the  coronaries  are  end- 
arteries  which  practically  do  not  anastomose,  has  been  in  a  strict 
sense  disproved  by  the  researches  of  Hirsch  and  Spalteholtz,  ^  Jannin 
and  Merkel;-  and  although  cases  have  been  reported  in  which 
occlusion  of  large  arteries,  such  as  the  right  coronary,  may  occur 
without  subsequent  myocardial  change  (Marchiafava,^  Chiari); 
and  although  the  last-named  arterj^  has  been  ligated  in  man  with- 
out subsequent  muscular  degeneration  (Pagenstecher^),  yet  these 
cases  are  exceptional,  and  must  be  explained  as  due  to  anomalous 
blood-supply  or  incomplete  occlusion.  Cases  of  the  opposite 
sort  have  also  been  noted,  as,  for  instance,  that  of  F.  T.  Stewart, 
in  which  a  human  heart  sutured  some  years  before  for  trauma, 

'  Hirsch  and  Spalteholtz:  Deut.  med.  Woch.,  1907,  p.  790. 

-  Jannin  and  Merkel:  Die  Koronararterien  des  Mensehliohen  Herzen,  etc.,  Jena,  1907. 
^  Marchiafava:   Revist.  critica  di  olin.  med.,  1904. 
■"  Pagenstecher:  Deut.  med.  Woch.,  1901,  p.  .56. 


Fid.  03. — C.\RDi.\c  Aneurism  and  Thrombosis. 
Thf  iiiusculatiiro  of  Iho  left  vontricle  near  the  apex  i.s  thinned  and  stretehed;   its  chamber 
is  nearly  filled  with  a  large,  dark,  jiilisteninp;,  adherent  thrombus,  which  shows  the  "Unes  of 
Zahn."     The  mitral  valve  is  moderately  .sclerosed.     (Photograph  by  Dr.  Alfred  R.  Allen.) 


182  STUDIES  IN  CARDIAC  PATHOLOGY 

disclosed  a  fibroid  myocarditis  originating  at  the  site  of  the  original 
ligature. 

When  the  coronary  arteries  are  ligated  in  animals,  death  may 
occur  suddenly,^  preceded  by  fibrillation,  or  it  ma}^  occur  in  the 
course  of  minutes,-  hours, ■'  or  weeks.'' 

But  we  must  bear  in  mind  tiiat  in  animals  we  are  dealing  with  healtliy  liearts 
wliich  we  Ivnow  are  able  to  sustain  a  great  deal  of  traumatic  insult.  Embolic  or 
thrombotic  manifestations,  on  the  other  hand,  rarely  occur  in  conjunction  with 
a  previously  healthj^  myocardium. 

Based  on  original  investigation  and  a  review  of  the  literature,  Amenomiya " 
draws  the  following  conclusions  regarding  the  coronary  arteries  and  the  papillary 
muscles.  The  7^ight  coronary  artery  supplies  the  greater  part  of  the  right  heart, 
the  posterior  part  of  the  ventricular  septum,  and  part  of  the  posterior  part  of 
the  left  heart.  The  left  coronary  artery  supplies  the  most  of  the  left  heart,  the 
anterior  part  of  the  ventricular  septum,  and  part  of  the  anterior  wall  of  the  right 
heart.  In  the  papillary  muscles  the  terminal  bifurcations  occur  as  straight, 
longitudinal,  and  radiating  branches.  The  anterior  papillary  muscle  of  the  left 
ventricle  is  supplied  solely  by  the  ramus  descendens  of  the  left,  and  the  posterior 
by  both  branches  of  both  coronary  arteries.  The  large  anterior  papillary  muscle 
of  the  right  ventricle  derives  its  nourishment  from  both  arteries,  the  branch  from 
the  left  artery  being  given  off  relatively  high  up  from  the  ramus  descendens. 
The  vessels  supplying  the  papillary  muscles  double  upon  themselves  upon  enter- 
ing, thus  describing  a  considerable  curve.  The  foregoing  anatomic  facts,  which 
are  unfavorable  to  perfect  circulatory  efficiency,  explain  why  the  papillary  muscles, 
especially  the  anterior  ones,  are  so  frequently  the  seat  of  infarction  and  fibrosis. 
It  has  been  shown  that  during  acute  infections  the  coronary  arteries  show  patho- 
logic alterations  before  the  other  vessels  of  the  body,  and  that  the  structural 
damage  thus  produced  maj^  lead  to  arteriosclerosis." 

Pathogenesis. — The  effects  of  arteriosclerosis  of  the  coronary 
arteries  may  be  due  either  to  disease  of  the  artery  itself  through- 
out its  course,  or  to  constriction  of  its  orifice  resulting  from  disease 
of  the  aorta.  The  types  of  coronary  arteriosclerosis  are  similar 
to  those  affecting  other  arteries — localized  or  general  thickening, 

'  Magrath  and  Kenned}':  Jour.  Exper.  Med.,  1S97,  p.  1.3.  Porter:  .Jour.  Physiol.,  1893, 
p.  121. 

-  Cohnheim  and  v.  Schulthess  Rechberg:  Arch.  f.  path.  Anat.,  1881,  p.  503. 

'  Panum:   Ibid.,  1863,  pp.  308,  433. 

■•  Baumgarten:  Am.  Jour.  Physiol.,  1899,  p.  243. 

^Amenomiya:  Virchow's  Arch.,  1910,  cic,  187. 

"Wiesel:  Wien.  kUn.  Woch.,  1906,  No.  26.  Wiesner:  Centralb.  f.  med.  Wissensch., 
1907,  No.  3. 


Fig.  64. — Aneurism  op  the  Left  Ventricle. 

The  left  ventricular  wall,  which  is  elsewhere  hypertrophied,  is  markedly  attenuated  on  its 
left  .side  at  and  above  the  apex.  In  this  region  a  marked  bulging,  about  the  size  and  shape  of  a 
large  duck  egg,  is  seen.  The  endocardium  in  this  region  is  covered  with  calcareous  plaques. 
The  aortic  and  mitral  valves  show  moderate  sclerosis.  (Specimen  from  the  Philadelphia 
Ho.spital.     Vol.  XV,  p.  39.     Phy.sician:   Dr.  F.  P.  Henry.) 


184  STUDIES    IN    CARDIAC    PATHOLOGY 

roughening,  hardening,  or  actual  calcification  being  met  with. 
On  account  of  the  smaller  cahber  of  some  of  the  branches,  occlusion 
may  readily  occur  and  thrombosis  result,  especially  if  the  blood- 
pressure  is  lowered  or  the  orifices  are  constricted.  Such  constric- 
tion is  of  frequent  occurrence.  Up  to  thirty  years  of  age  the  elastic 
tissue  in  the  aorta  increases.^  Both  Adami  and  Aschoff  regard 
this  as  a  work  hypertrophy.  For  the  following  fifteen  years  the 
amount  of  this  connective  tissue  remains  stationary.  After 
fift}^  3'ears  there  is  a  slow,  progressive  wasting  of  the  elastica, 
and  a  stretching  and  thinning  of  the  media  occurs.  "The  domi- 
nant primary  event  in  the  arteriosclerotic  process — syphilitic, 
senile,  functional — is  a  localized,  or  it  may  be  diffuse,  weakening 
of  the  arterial  wall,  and  especially  of  the  media.  This  induces 
increased  strain  upon  the  remaining  coats;  and  if  this  be  not 
excessive,  that  strain  leads  more  especially  to  connective-tissue 
overgrowth  and  the  development  of  the  characteristic  lesions  of 
arteriosclerosis"  (Adami).  Syphilitic  disease  of  the  aorta  is  a 
relatively  frequent  manifestation  of  this  infection.  It  is  apt  to 
occur  early  in  life,  to  be  of  a  serious  and  progressive  nature,  and, 
as  already  pointed  out,  to  affect  just  that  portion  of  the  aorta 
from  which  the  coronary  arteries  arise.  In  addition  to  lues, 
certain  acute  infections,  such  as  typhoid  and  rheumatic  fevers, 
and  certain  chronic  infections,  such  as  rheumatoid  arthritis,  often 
seem  to  produce  arteriosclerosis. 

Three  more  or  less  distinct  types  of  arteriosclerosis  of  the  larger  vessels 
occur  in  man:  (1)  The  ordinary  nodular  form;  (2)  dilatation  of  the  vessels  with 
increased  tortuosity,  the  peripheral  arteries  being  of  the  "pipe-stem"  variety, 
and  (3)  the  syphilitic  type,  affecting  chiefly  the  ascending  aorta,  in  which  the 
nodules  eventuallj^  cause  depressions  in  the  intima.  This  is  primarily  a  mes- 
aortitis,  with  wasting  of  the  media,  and  with  thickening  of  the  other  coats. 

In  1,000  consecutive  autopsies  Brooks-  found  coronary  sclerosis  of  sufficient 
degree  to  "seriously  affect  the  nutrition  of  the  heart  "  in  270  cases.  The  earliest 
instance  occurred  in  a  boy  of  fifteen  years,  the  average  age  being  forty-five  years. 
The    following   associated    conditions   were    found:  Chronic   alcoholism,    107;. 

'  Foster:  Jour.  Med.  Research,  Sept.,  1909. 
-  Brooks:  New  York  Med.  Jour.,  1906,  p.  825. 


Fig.  6.5. — Ball  Thkombus  in  the  Left  Auricle. 
A  largo,  dark,  ball-shaped  thrombus  lies  free  in  the  left  auricular  cavity.     Numerous 
smaller  mural  thrombi  are  seen  enmeshed  in  the  columna;  cameae  and  chorda;    tendinea;. 
The  left  ventricular  wall,  which  is  elsewhere  hypertrophied,  is  noticeably  thinned  near  the 
ape.x.     fPhotOKraph  by  Dr.  .Vlfred  R.  Allen.) 


186  STUDIES   IN    CARDIAC    PATHOLOGY 

nephritis,  35;  syphilis,  30;  tuberculosis,  20;  carcinoma,  1;  diabetes,  6;  plumb- 
ism,  2.  All  but  15  showed  macroscopic  myocardial  lesions.  In  215  cases  these 
changes  were  sufficient  to  be  considered  as  contributory  to  the  cause  of  death. 
The  following  lesions  were  observed:  Brown  atrophy,  64;  fibrosis,  24;  hyper- 
trophy, 35;  acute  dilatation,  20;  aneurism,  2;  cardiac  rupture,  2.  At  the 
Philadelphia  General  Hospital,  which  is  very  rich  in  such  material,  among  8,640 
autopsies  the  following  myocardial  lesions  were  encountered :  Acute  suppurative 
myocarditis,  5;  myocardial  thrombosis,  28;  sarcoma,  4;  carcinoma,  4.  At  the 
Pennsylvania  Hospital  among  1,300  autopsies  there  was  1  case  of  coronary 
aneurism  and  10  cases  of  coronary  obhteration.     (See  page  48.) 

Arteriosclerosis  of  the  coronary  artery  is  the  commonest  pathologic  finding 
in  cases  of  angina  pectoris. 

Among  83  cases  of  angina  pectoris  Bouchard  found  only  12  with  a  history 
of  syphilis.  Among  261  syphilitics,  4.5  per  cent,  suffered  from  angina  pectoris; 
among  3,739  non-syphilitics,  only  2  per  cent.  did.  Of  the  above  mentioned  261, 
14  per  cent,  presented  aortic  lesions.^ 

The  left  coronary  artery  generally  shows  the  most  marked  sclerotic  changes. 
These  appear  as  localized  or  diffuse  thickening,  especially  at  the  points  of  bi- 
furcation or  branching.  Partial  occlusion  generally  results  in  myomalacia  cordis, 
which,  if  several  contiguous  areas  are  involved,  results  in  aneurismal  dilatation. 

The  localization  and  extent  of  arteriosclerosis  is  to  a  certain  extent  depen- 
dent upon  functional  activity.  Boveri's  ^  experiments  on  animals  tend  to  con- 
firm the  clinical  view  that  hard  muscular  work  leads  to  arteriosclerosis.  In 
laborers  the  location  of  the  most  pronounced  vascular  lesions  corresponds  to  the 
part  of  the  body  which  performs  most  of  the  work — the  lower  extremities  in 
knife-grinders,  the  upper  extremities  in  wood-  and  stone-cutters.  It  is  not  im- 
probable that  fatigue  toxins  have  some  effect.  It  has  sometimes  been  possible 
to  determine  post  mortem  by  the  amount  of  arteriosclerosis  which  organ  of  the 
body  functionated  most  actively  during  life.'  An  inchcation  that  such  arterio- 
sclerosis may  be  the  result  of  increased  blood-pressure  may  be  found  in  the  fact 
that  rabbits  suspended  by  the  hind  legs  for  three  minutes  daily  over  a  period  of 
one  hundred  and  twenty  days  showed  well-marked  arterial  lesions  in  the  upper 
part  of  the  body.^  A  normal  pressure  with  weakened  media,  or  an  increased 
pressure  with  a  normal  media,  may  cause  a  giving  way  of  the  arterial  coat  with 
secondary  intimal  changes.  To  a  certain  extent  the  toxins  of  disease  exert  a 
specific  selective  action.  Klotz  and  Saltykow^  have  shown  that  diphtheria 
affects  the  media,  while  the  typhoid  fever  exerts  its  noxious  influence  on  the 
intima. 

That  syphilis  is  one  of  the  commonest,  if  not  the  commonest,  causes  of 
sclerosis  of  the  aorta  cannot  be  doubted.     In  a  study  of  54  cases  byBittdorf' 

'  Arch,  du  Mai  du  Coeur,  1909,  p.  98. 

=  Boveri:   Riforma  Medica,  1909,  No.  30,  31. 

'  Askana:  Therapeut.  Monatshefte,  Sept.,  1907. 

••  Klotz:  Quoted  Adami,  Am.  Jour.  Med.  Sci.,  Oct.,  1909. 

»  Saltykow:   Ziegler's  Beitriige,  1908,  xlii,  187. 

»  Bittdorf :  Deut.  Arch.  f.  klin.  Med.,  Ixxxi,  1904,  No.  122. 


CARDIAC    DILATATION  187 

the  average  age  at  which  this  lesion  occurred  was  55.6;  in  syphihtics  the  average 
age  was  ten  years  younger.  Huchard'  in  a  study  of  1,835  cases  of  arterio- 
sclerosis seen  in  private  practice  found  a  history  of  gout  in  323,  of  rheumatism 
in  332,  of  syphilis  in  209,  of  the  abuse  of  tobacco  in  181,  of  infectious  disease 
in  67,  of  alcohol  in  27. 

Although  the  arteriosclerosis  produced  by  means  of  adrenalin,  barium 
chlorid,  nicotin,  etc.,  differs  from  that  which  occurs  spontaneously  in  man, 
inasmuch  as  in  the  former  the  changes  are  hmited  almost  entirely  to  the  mecUa, 
yet  both  of  these  types  have  as  a  common  basis  a  giving  way  of  the  media. 
Adami  suggests  that  the  intimal  changes  are  lacking  in  the  experimental  variety 
on  account  of  their  acuteness,  and  considers  that  the  arterial  thinning  of  the 
Monkeberg  type,  and  the  intimal  thickening  of  senile  arteriosclerosis,  are  diverse 
manifestations  of  a  common  process. 

'Huchard:  Bull,  de  I'acad.  d.  Med.,  July  1.5,  190S. 


XL  CARDIAC  ANEURISM 

Aneurism  of  the  myocardium  consists  of  a  localized  bulging  of 
the  heart,  and  is  brought  about  through  stretching  of  the  softened 
muscle  or  the  fibrous  tissue  which  displaces  a  diseased  myocardium. 
At  times  the  septum  is  involved.  Rarely  the  aneurism  is  an 
extension  of  the  aneurismal  dilatation  of  one  of  the  valves,  e.  g., 
the  mitral,  with  secondary  involvement  of  the  wall  of  the  heart. 

The  fibroid  degeneration  which  precedes  the  aneurism  may 
result  from  coronary  sclerosis,  either  the  mouths  or  the  terminal 
branches  of  these  vessels  being  diseased.  Chronic  endocarditis 
and  the  traction  of  pericardial  adhesions  are  also  causative  factors 
in  some  instances.  Cardiac  aneurism  is  distinctly  rare,  and  except 
in  those  cases  where  rupture  produces  hemopericardium  and  sudden 
death,  it  is  often  discovered  unexpectedly  at  autopsy.  (See 
"Coronary  Sclerosis,"  p.  180.) 

The  condition  is  generally  single,  although  multiple  aneurisms 
have  been  noted.  The  myocardium,  which  may  be  greatly 
thinned  and  stretched,  is  replaced  to  a  greater  or  less  extent  by 
fibrous  tissue.  At  times  the  opening  into  the  aneurism  is  con- 
stricted and  forms  a  dilated  sac  beyond,  but  this  is  not  generally 


Fig.  66. — Rupture  of  the  Aorta. 

M.  S.,  male,  white,  aged  fifty-one  years.  (Philadelphia  Hospital.  Autopsy  vol.  xix,  p. 
281.     Physician:  Dr.  Mills.     Pathologist:  Dr.  J.  D.  Wilson.) 

Clinical  Notes:  Arrhythmia;  pulse  90.  Sudden  death,  with  marked  cyanosis  and 
rigidity  of  the  body. 

Pathologic  Diagnosis:  Rupture  of  the  aorta;  chronic  interstitial  nephritis,  with  acute 
exacerbation;   nutmeg  liver;   general  arteriosclerosis. 

Pericardium:  Extends  from  the  right  border  of  the  sternum  to  the  left  axillary  line.  On 
incision,  blood  spurts  freel}'.  The  cavity  contains  1,000  c.c.  of  fluid  blood,  and  an  equal  amount 
of  blood-clot. 

Heart:  Weighs  750  gm.,  has  a  normal  color.  Myocardium  is  thickened  and  firm.  Endo- 
cardium normal  except } or  small  patch  of  atheroma  on  the  aortic  valve,  hi  the  aorta,  2  c.c.  above 
the  valve  margin,  there  are  two  openings,  one  a  vertical  slit  3  cm.  long,  which  forms  an  opening 
from  the  aorta  to  the  pericardial  cavity.  The  other,  6  cm.  long,  is  situated  directly  opposite,  but 
extends  only  to  the  connective  tissue  surrounding  the  vessel.  This  tissue  surrounding  the  lateral 
slit  is  markedly  reddened  and  swollen. 

1S8 


190  STUDIES  IN  CARDIAC  PATHOLOGY 

the  case.  Aneurisms  are  generally  found  on  the  anterior  surface 
of  the  left  ventricle  above  the  apex.  Such  dilatation  has  clinically 
simulated  a  pericardial  effusion  to  such  an  extent  that  aspiration 
was  performed  and  blood  withdrawn  from  the  left  ventricle.^ 
Among  the  1,300  Pennsylvania  Hospital  autopsies  there  were  5 
cases  of  cardiac  aneurism;  at  the  Philadelphia  Hospital,  3  among 
8,640.     Legg  found  3  in  1,899  autopsies. 

To  parietal  endocarditis  has  also  been  ascribed  an  etiologic 

'  W.  Pepper:   University  of  Penna.  Med.  Bull.,  vol.  i. 


Fig.  67. — Gummas  op  the  Myocardium.     (Right  heart.)     (See  also  Fig.  68.) 

Male,  aged  thirty-eight  years.  (Pennsylvania  Hospital.  Specimen  239.  Physician: 
Dr.  A.  V.  Meigs.) 

Clinical  Notes  :  Patient's  health  had  been  poor  for  the  last  few  years;  he  had  complained 
of  frequent  micturition  and  asthma.  He  at  one  time  had  swelling  of  the  feet.  Before  the 
present  attack  he  had  no  distinct  convulsions,  but  had  had  frequently  what  he  called  "spells." 
He  denied  ever  having  had  syphilis.  At  the  time  of  his  admission  to  the  hospital  he  was  in  a 
state  of  partial  collapse,  with  cyanosis,  cold  extremities,  vomiting,  and  retching.  The  heart 
action  was  "excessively  slow"  and  irregular,  "there  being  when  the  patient  first  came  into 
the  ward  two  or  three  respirations  taken  for  each  beat  of  the  heart."  There  was  a  loud  blow- 
ing murmur  at  the  apex.  On  the  day  following  the  patient  frequently  complained  of  feeling 
faint,  and  during  these  attacks  objects  swam  before  his  eyes.  Cyanosis  and  cold  extremities 
were  constant.  The  murmur  still  persisted,  but  was  heard  louder  at  the  base  of  the  heart. 
Pulse  34,  respirations  18,  temperature  98°  F.  Five  days  later  the  patient  uttered  a  shriek  and 
died  suddenly. 

Pathologic  Report:  "The  specimen  shows  a  heart  with  a  firm,  nodular  mass  situated 
in  the  septum  and  reaching  from  the  tricuspid  valve  into  the  right  auricle,  and  also  making  a  pro- 
jection into  the  left  ventricle  just  below  the  aortic  orifice;  its  size  is  about  that  of  a  walnut.  In  the 
right  auricle  it  juts  forward  directly  over  the  tricuspid  orifice,  and  in  the  left  ventricle  it  in- 
volves nearly  the  whole  of  the  ventricular  surface  of  the  aortic  cusp.  Its  tissue  is  firm,  some- 
what elastic,  and  on  section  shows  a  pretty  uniform  consistence  and  a  gray  color.  Numerous 
firm  clots  are  entangled  in  the  columna?  carneaj  of  the  right  ventricle,  which  are  continuous 
through  the  tricuspid  orifice  and  pulmonary  artery.  The  organ  weighs  17  J^  ounces.  A  micro- 
scopic examination  showed  the  characteristic  appearance  of  a  syphilitic  gumma."  (Meigs.') 
"Further  examituiUmi  of  llu'  preserved  specimen  shows  that  this  nodular  mass  obliterates  the  un- 
defended space  «/  /lie  lull  rreiilrindur  septum,  and  entirely  fills  that  part  of  the  septum  through 
which  the  auricalu-eeiUneidar  bundle  runs.  It  is  the  posterior  leaflet  of  the  aortic  valve  into 
which  the  gumma  has  grown.  To  the  right  of  this  leaflet  there  is  a  small  second  nodule 
10  X  7  mm.  The  root  of  the  aorta  is  corrugated  and  appears  to  be  the  seat  of  a  syphilitic 
aortitis."     (Robinson.) 

There  is  every  reason  to  believe  (although  this  case  was  first  reported  long  before  the 
existence  of  the  auriculo- ventricular  bundle  was  known,  or  its  function  understood)  that  we 
had  here  to  deal  with  a  case  of  auriculo-ventricular  heart  block  due  to  a  gumma  of  the  myocar- 
dium involving  the  interventricular  septum. 

'  This  case  was  reported  by  Dr.  A.  V.  Meigs  in  the  Transactions  of  the  College  of  Physicians 
of  Philadelphia,  1881,  third  series,  vol.  v;  further  studied  and  reported  by  Dr.  G.  C.  Robinson 
in  the  Bulletin  of  the  Ayer  Clinical  Laboratory,  1907,  No.  iv. 


192  STUDIES  IN  CARDIAC  PATHOLOGY 

role.^  Such  a  case  has  recently  been  reported  by  Bret  and  Rou- 
bier.-  Cardiac  aneurism  may  also  result  from  traumatic  scar 
formation,  suppurative  foci,  or  gummatous  myocarditis. 

According  to  M'Elroy,^  there  are  now  on  record  in  medical 
literature  some  300  cases  of  myocardial  aneurism.  Warthin 
states  that  the  condition  may  be  congenital.  Among  208  cases 
collected  by  Hare,  74  per  cent,  occurred  in  men.  Only  about 
7  per  cent,  of  the  chronic  cases  terminate  in  rupture. 

Actual  calcification  of  the  myocardium  is  distinctly  rare, 
and  its  pathology  not  thoroughly  understood.  Apparently  the 
calcification  occurs  as  a  sequel  to  muscular  degeneration.  Hart,^ 
who  has  collected  13  cases,  has  suggested  that  hyaline,  glycogenic, 
and  amyloid  changes  may  be  the  real  substratum  of  the  condition. 
Topham  has  reported  actual  bone  formation  in  the  heart  of  a 
man  dying  at  the  age  of  seventy-one.'' 

CARDIAC  THROMBOSIS 

"The  term  cardiac  thrombosis  must  be  reserved  for  a  solid  or 
partly  solid  structure,  primarily  formed  from  the  blood-elements, 
which  develops  in  one  or  more  of  the  heart  chambers  during  life. 
Such  a  mass  may  be  attached  to  the  cardiac  wall  by  a  more  or 
less  altered  base,  or  may  exist  as  a  free  foreign  body  within  a  heart 
cavity.  When  cardiac  thrombi  are  measured  bj^  this  standard 
they  are  uncommon  post-mortem  findings.'"^  For  the  production 
of  cardiac  thrombosis  three  factors  are  necessary:  first,  local 
endocardial  injury — mechanical,  bacterial,  or  toxic;  second, 
an  increase  of  hemagglutinins  in  the  blood;  and,  third,  slowing 
of  the  blood-stream.  Thrombi  are  met  with  in  valvular  heart 
disease,  in  cachectic  states,  and  in  blood  dyscrasias.  In  the  first- 
named  class  they  maj^  begin  as  vegetations.     Infectious  diseases 

1  Strauch;  Zeit.  f.   klin.  Med.,  1900,  p.  231. 

-  Bret  and  Roubier:  Arch.  d.  Mai.  du  Cceur.,  1910,  p.  445. 

'  M'Elroy:  Jour.  Am.  Med.  Assoc,  Aug.  1,  1908. 

•"  Hart:  Zeit.  f.  Patholog.,  1909,  iii,  706. 

'^Topham:  Brit.  Med.  Jour.,  Oct.  1.3,  1906. 

"Smithies:   Jour.  Am.  Med.  Assoc,  1909,  p.  1347. 


Fic.  OS. — Gummas  of  the  Myocardium.     (Left  heart.)     (See  legend  under  Fig.  67.) 


194  STUDIES  IN  CARDIAC  PATHOLOGY 

except  influenza  and  tuberculosis  are  rarely  complicated  by  throm- 
bosis. The  most  common  site  is  in  the  left  auricle,  the  right  auricle 
and  the  left  ventricle  coming  next  in  frequency,  while  "primary 
thrombosis  of  the  right  ventricle  appears  to  be  unknown." 

Thrombosis  is  probably  more  common  in  mitral  stenosis  than 
in  any  one  other  condition.  It  is  also  met  with  in  cardiac  dilata- 
tion, especially  when  sclerotic  endocardial  or  myocardial  changes 
are  present.  Hence  it  is  more  common  in  the  later  years  of  life, 
although  it  has  been  described  in  childhood.  The  shape  of  the 
thrombi  varies  considerably,  but  generally  they  can  be  classified 
either  as  pedunculated  or  of  the  ball  variety,  the  former  being 
the  more  common.  The  effect  of  cardiac  thrombosis  upon  the 
circulation  is  generally  marked.  Such  a  condition  interferes 
considerably  with  cardiac  contraction  and  with  the  transference 
of  blood  from  one  chamber  to  another,  so  that  from  a  diagnostic 
standpoint  the  severity  of  the  symptoms  is  out  of  all  proportion 
to  the  apparent  degree  of  the  cardiac  lesion.  At  the  Pennsylvania 
Hospital  there  were  6  cases  in  1,300  autopsies;  at  the  Philadelphia 
Hospital,  28  among  8,640. 

Cardiac  rupture  may  occur  as  the  result  of  fatty  degeneration, 
aneurismal  dilatation,  suppurative  myocarditis,  acute  necrosis, 
gummatous  disease,  and  brown  atrophy.  This  condition  was 
first  described  by  Harvey,  and  later  by  Morgagni.  Among 
Quain's  100  collected  cases  77  were  due  to  fatty  degeneration. 
Most  of  the  patients  were  beyond  sixt.y  years  of  age,  and  sudden 
death  occurred  in  71  per  cent.  The  site  of  rupture  was  as  follows: 
Left  ventricle,  55;  right  ventricle,  7;  right  auricle,  3;  left  auricle,  2. 
Rupture  may  be  complete  or  incomplete.  It  is  slightly  more 
frequent  in  males.  In  18  of  LetuUe's  110  cases,  multiple  rupture 
was  found.  Occasionally  rupture  occurs  in  apparently  healthy 
young  people  as  the  result  of  coronary  thrombosis.^  Quain's 
cases  included  two  between  the  ages  of  ten  and  twenty.     Rupture 

■  Klingmann:   New  York  Med.  Jour.,  190S,  p.  199. 


Fig.  69. — Gumma  of  the  Myocardium. 

A  larfcc,  firm,  nodular  mass  is  seen  in  the  septum  below  the  aortic  valves  which  bulges 
forward  into  the  ventricle.  Another  mass  is  seen  in  the  wall  of  the  ventricle.  These  masses 
were  firm,  .slightly  elastic,  grayish  in  color,  and  upon  microscopic  examination  showed  typical 
gummatous  structure. 

The  heart  is  that  of  a  patient  aged  thirty-one  years,  who  had  contracted  syphilis  eight 
years  before.  Three  years  previous  to  admission  he  had  been  incapacitated  for  three  days 
by  an  "inflammation  of  the  heart."  Six  weeks  before  admission  he  had  had  fugacious  pains 
and  less  of  power  in  the  right  hand.  A  few  days  afterward  he  had  a  syncopal  attack  while  at 
work,  following  which  he  developed  headache,  weakness,  numbness  of  the  legs,  and  diplopia. 
On  admi.s.sion  to  the  hospital  he  was  found  to  have  a  right-sided  hemiplegia.  On  auscultation 
a  mitral  systolic  murmur  was  noted.  During  his  three  months'  stay  in  the  hospital  he  had 
hemoptysis  and  cardiac  pain.     (Pennsylvania  Ho.spital,  No.  .301.     Dr.  J.  M.  DaCosta.) 


196  STUDIES  IN  CARDIAC  PATHOLOGY 

of  a  'papillary  muscle  is  extremely  rare.  Dennig^  has  reported  a 
case,  and  alludes  to  the  scanty  literature  on  the  subject.  It 
may  follow  great  increase  of  blood-pressure,  especially  with  a 
diseased  myocardium,  or  it  may  result  from  crushing  trauma 
of  the  thorax  or  from  ulcerative  processes.  Spontaneous  car- 
diac rupture  is  to  be  differentiated  from  the  traumatic  variety 
— the  question  is  often  of  medico-legal  importance — as  follows: 
The  former  occurs  chiefly  in  advanced  years;  the  parietal  peri- 
cardium shows  no  lesion,  the  heart  muscle  near  the  site  of 
the  tear  generally  does.  The  tear  is  usually  near  the  apex  in  the 
left  ventricle,  and  assumes  a  zigzag  outline.  Although  it  has  been 
stated  that  a  perfectly  normal  heart  may  rupture  under  great 
strain,  this  is  very  questionable.  Such  cases  probably  always  have 
a  preceding  pathologic  basis  which  predisposed  to  the  rupture 
(ThoreP).  Geill,^  in  an  analysis  of  90  cases  of  traumatic  cardiac 
rupture  produced  by  blows  delivered  with  dull  instruments,  etc., 
found  the  right  ventricle  frequently,  and  the  left  rarely,  injured. 
There  is  much  discrepancy'  of  opinion  as  to  whether  the  tearing, 
crushing,  or  bursting  element  is  the  most  important  in  the  mechan- 
ism of  traumatic  rupture.  The  mode  of  death  in  such  cases  de- 
pends upon  whether  the  exudation  of  blood  into  the  pericardial 
sac  is  sudden  or  gradual.  In  the  former  we  may  have  an  actual 
mechanical  compression — "tamponade";  in  the  latter  a  gradual 
interference  with  diastole  through  the  secondary  effect  of  the  de- 
pressor nerve  on  the  vasomotor  center  (Placzek*).  In  the  former 
the  pericardium  will  be  tensely  distended  and  the  heart  collapsed; 
in  the  latter  both  of  these  conditions  will  be  less  marked. 

The  distribution  of  cardiac  rupture  among  8,640  autopsies  at 
the  Philadelphia  Hospital  was  as  follows :  One  of  the  left  ventricle, 
two  of  the  left  auricle,  one  of  a  papillary  muscle. 

■  Dennig:   Deut.  Arch.  f.  klin.  Med.,  1909,  p.  163. 
^Thorel:  Lubarsch  and  Ostertag's  Ergebnisse,  1907,  ii,  425. 
'  Geill:  Viertel  Jahrschr,  f.  Gericht.  Med.,  189.5,  xvii. 
^Placzek:   Ibid.,  1902. 


Fif;.  70. — fliMMA  OF  THE  T,i;iT  \'jc\Tniri.K.      (Specimen  I'rom  the  Fonnsylvania  Hosiiital.) 


198  STUDIES    IN    CARDIAC    PATHOLOGY 

Among  132  cases  Odriozola^  found  the  site  of  the  rupture  to  be 
as  follows:  Left  ventricle,  96;  right  ventricle,  22;  left  auricle, 
2;    auriculo-ventricular  groove,  2. 

The  size  of  the  tear  in  the  spontaneous  cases  varies,  but  is 
generally  from  one-half  to  one  inch  in  length.  Not  infrequently 
the  tear  is  larger  on  the  outside  than  on  the  inside.  The  rupture 
is  often  that  of  an  "X"  or  a  "Y."  Ruptures  generally  occur 
during  muscular  strain,  but  may  do  so  during  sleep.  As  a  historic 
example  it  may  be  recalled  that  George  the  Second  died  of  a 
ruptured  right  ventricle. 

Spontaneous  rupture  of  the  aorta  without  preceding  aneurismal 
dilatation  is  occasionally  met  with.  It  generally  occurs  in  the 
aged,  and  is  associated  with  atheromatous  or  sclerotic  vascular 
disease,  but  at  least  two  cases  have  been  reported  in  children 
under  fourteen  years  of  age  in  whom  the  aorta  showed  only  yery 
slight  evidences  of  disease,  on  account  of  which  a  congenital  weak- 
ness of  this  structure  was  assumed. - 

TUMORS  OF  THE  HEART 

Primary  neoplasms  of  the  heart  are  extremely  rare.  There 
were  no  such  cases  among  the  9,940  autopsies  studied  by  the 
author,  nor  among  3,000  reviewed  by  Thorel.^  Of  110  cases  of 
heart  tumors  found  in  the  Index  Catalogue  of  the  Surgeon-General's 
Library  the  majority  were  secondary.  The  mesoblastic  origin  of 
the  heart  accounts  for  preponderance  of  sarcomata  (Hektoen*). 
A  recent  compilation  of  cases  by  Link"  shows  the  following 
data:  total  number  of  primary  heart  tumors,  91.  Among  61  of 
these  the  character  of  the  growths  was  as  follows:  Sarcoma,  13; 
myxoma,  18;  carcinoma,  7;  lipoma,  8;  myoma,  5;  rhabdomyoma, 
1;   teratoma,    1;    papilloma,    1.     The   growths   were   distributed: 

'  Odriozola:   Etude  sur  le  cocur  senile,  Paris,  18S8. 

=  The  literature  on  this  subject  can  be  found:  Berge:  Gaz.  d.  Hopit.,  1906,  No.  38.  Thorel: 
Lubarsch  and  Ostertag's  Ergebnisse  d.  allg.  Path.,  1907,  ii,  577. 

'  Thorel:  Lubarsch  and  Ostertag's  Ergebnisse  d.  allg.  Path.,  1903,  pt.  1;   1907,  pt.  2. 
'Hektoen:   Med.  News,  1893,  p.  571. 
5  Link:   Zeit.  f.  klin.  Med.,  1909,  p.  272. 


CARDIAC    ANEURISM  199 

Left  auricle,  24;  valves,  16;  right  ventricle,  14;  right  auricle,  10; 
left  ventricle,  8;  interauricular  septum,  2;  both  auricles,  3; 
both  ventricles,  2;  right  auricle  and  ventricle,  2;  left  auricle 
and  ventricle,  2;  at  the  junction  of  the  auricular  and  ventricular 
septa,  2.  In  the  foregoing  study  gummas,  cysticerci,  and  secondary 
tumors  were  excluded.  The  age  of  the  patients  in  Schoeppler's 
series  ranged  from  three  days  to  eighty-three  years.  ^  It  has  quite 
frequently  happened  that  the  heart  has  manifested  very  few  symp- 
toms of  insufficiency  even  with  extensive  mj^ocardial  involvement.^ 

'  Schoeppler:   Miinch.  med.  Woch.,  1906,  liii,  No.  45. 

-  Another  case  of  sarcoma  has  recently  been  reported  by  Ehrenberg,  Upsala,  Lakarefoerings 
ForhandUngar,  1910,  xv. 


XII.  CARDIAC  SYPHILIS 

Occurrence. — SjqDhilis  of  the  heart  was  first  described  by 
Ricord  in  1845.  Virchow  distinguished  two  distinct  types: 
(a)  gumma  formation;  (6)  diffuse  interstitial  change.  In  1904 
Stockman  collected  80  cases  of  the  former  type.  Mracek  has 
published  the  pathologic  findings  of  102  cases,  he  having  found 
4  cases  of  cardiac  syphilis  among  150  autopsies.  Loomis  found 
4  cases  in  1,500  autopsies,  and  describes  amyloid  change  resulting 
from  this  infection.  Among  61  of  Mracek's  cases  gummas  oc- 
curred in  about  50  per  cent.  Any  part  of  the  myocardium, 
endocardium,  or  pericardium  may  be  involved.  A  considerable 
number  of  cases  of  the  Adams-Stokes  syndrome  showing  gumma- 
tous lesion  in  the  auriculo-ventricular  bundle  are  now  on  record. 
The  Pennsylvania  Hospital  statistics  showed  2  cases  in  1,300 
autopsies;   the  Philadelphia  Hospital  records,  1  in  8,640. 

Pathologic  Anatomy. — Gtimmatous  cardiac  disease  consists  of 
circumscribed  tumor-like  masses  which  on  section  appear  dry  and 
yellowish  or  grayish  in  color.  The  lesions  are  chiefly  encountered 
in  the  ventricles,  though  the  auricles,  and  especially  the  inter- 
ventricular septum,  are  often  diseased.  The  involvement  is 
generally  multiple,  the  size  ranging  from  0.5  cm.  upward.  If 
breaking  down  occurs,  cardiac  sclerosis  or  aneurism  may  result. 
The  gummatous  cases  are  usually  accompanied  by  more  or  less 
diffuse  fibrous  change.  The  gummas  show  the  characteristic 
histologic  structure.  They  are  generally  sharply  defined  and 
encapsulated.  In  the  fibrous  type  involvement  of  the  endo- 
cardium and  the  pericardium  is  more  frequent  than  in  the  gum- 
matous variety.  As  might  be  expected,  vascular  changes  in  the 
coronary  vessels  are  common  findings.  Syphilitic  endocarditis 
and  pericarditis  are  generally  secondary  to  myocardial  disease. 
The  fibrous  type  of  cardiac  sj'philis  is  essentially  a  microscopic 

200 


Fiu.  71. — .Syphilitic  Aortitis. 

Syphilitic  me.saortitis  occurs  characteristically  about  one  and  one  half  inches  above  the 
aortic  valves,  often  spreading  downward  and  involving  the  mouths  of  the  coronary  arteries 
and  the  leaflets  secondarily.  The  surface  of  the  aorta  appears  depressed — not  elevated  as  in 
the  ordinary  arteriosclerotic  lesions.  It  is  a  prolific  source  of  aortic  aneurism,  and  aortic 
rupture.  (See  "Cardiac  Syphilis,"  p.  200,  and  "Diseases  of  the  Aortic  Orifice,"  p.  50. 
Compare  Figs.  41,  66,  72.; 


202  STUDIES    IN    CARDIAC    PATHOLOGY 

lesion.  It  is  of  considerable  rarity.^  Warthin  has  described 
diffuse  myocardial  fibrosis  due  to  congenital  syphilis,-  and  produc- 
tive mesaortitis  as  a  hereditary  lesion  has  been  reported  by  Bruhns,^ 
Wiesner,*  and  Klotz." 

That  mesaortitis  is  frequently  the  result  of  syphilis  has  been 
shown  by  the  demonstration  of  the  Spirochoeta  pallida  in  these 
lesions.''  The  lesion  is  generally  confined  to  the  arch  of  the  aorta, 
or,  as  in  the  case  depicted  in  Fig.  71,  extends  only  about  5  cm. 
above  the  aortic  valves.  It  is  definitely  localized  and  often  ab- 
ruptly circumscribed.  Longcope  found  21  cases  of  chronic  aortic 
endocarditis  without  involvement  of  the  other  valves  among  930 
autopsies  at  the  Pennsylvania  Hospital.  "In  the  least  extensive 
areas  there  were  patches  of  thickening  2  or  3  cm.  in  diameter. 
The  central  portion  was  elevated,  gray,  and  somewhat  succulent 
in  appearance,  while  the  margins  were  yellowish  and  crinkled. 
The  sclerosis,  when  more  extensive,  was  characterized  by  an 
irregular  corrugated  or  crinkled  thickening  of  the  wall,  showing 
small  pits  and  sometimes  minute  aneurismal  sacculations.  Often 
the  bases  of  these  small  aneurisms  were  so  thin  that  they  trans- 
mitted light.  There  was  no  calcification  except  in  one  instance, 
but  rather  a  rubbery  pliable  thickening.  In  4  cases  the  arch  of 
the  aorta  was  the  seat  of  large  aneurismal  formations.  The  valves 
showed  the  same  rubbery  thickening  when  extensively  involved, 
and  occasionally  there  were  crescentic  lines  of  whitish-yellow 
thickening  on  the  endocardium  of  the  ventricle  beneath  the 
valves."  The  diagnoses  in  these  cases  were  corroborated  by  mi- 
croscopic examinations,  and  extension  downward  into  the  aortic 

'  For  further  information  see  Mracek,  Arch.  f.  Dermat.  u.  Syphilis,  xxv,  1893,  Ergan- 
zungsheft,  p.  279;  Landois,  ibid.,  1908,  p.  221;  and  Stockmann,  "Ueber  Gummiknoten  in 
Herzfleische  bei  Erwachsenen,"  Wiesbaden,  1904. 

-Warthin:  Trans.  Assoc.  Am.  Phys.,  1910. 

'  Bruhns:   BerUn.  klin.  Woch.,  xUi,  No,  8. 

■I  Wiesner:  Centralbl.  f.  Path.  u.  path.  Anat.,  1905,  p.  822. 

^  Klotz:  Jour.  Path,  and  Bact.,  1907,  p.  11. 

"  Renter;  Mijnch.  med.  Woch.,  1906,  p.  778;  Ztsch.  f.  Hyg.  u.  Infektionskh.  1906,  p.  49. 
Benda:  BerUn.  khn.  Woch.,  1906,  p.  989.  Schmorl:  Munch,  med.  Woch.,  1907,  p.  188. 
Wright:  Boston  Med.  and  Surg.  Jour.,  1909,  p.  539. 


Fig.  72. — Syphilitic  Aortitis. 
In  thi.s  specimen  the  syphilitic  prooes.s  has  extended  downward  along  the  aortic  wall  and 
involved  the  coronary  orifices  and  the  aortic  leaflets.  The  smooth,  more  or  less  sharply  cir- 
cumscribed rubbery  appearance  of  the  lesions  is  shown.  Also  the  absence  of  calcification. 
(Compare  with  Fiss.  41,  66,  and  71.  See  also  under  "Cardiac  Syphilis,"  p.  200,  and  "Dis- 
easf»  of  the  .Vonif  Orififo,"  p.  50.) 


204  STUDIES  IN  CARDIAC  PATHOLOGY 

leaflets  suggested  that  "the  agent  which  produced  the  chronic 
inflammatory  and  proliferative  changes  in  the  wall  of  the  aorta 
had  some  part  in  the  disease  of  the  aortic  valves." 

Of  these  21  cases  all  but  3  had  shown  the  clinical  evidences  of  aortic  leakage. 
There  were  55  other  cases  of  aortic  endocarditis  among  the  930  autopsies 
in  which  the  etiologic  factor  was  an  antecedent  acute  endocarditis  (history 
of  infections  and  involvement  of  other  valves,  21  cases),  and  others  in  which  the 
sclerosis  was  general,  involved  the  whole  aorta,  and  was  associated  with  marked 
calcification  (endarteritis  deformans — pure  aortic  endocarditis,  34  cases).' 

'  Longcope:  "The  Association  of  Aortic  Insufficiency  with  Syphihs,"  .lour.  Am.  Med. 
Assoc,  .Ian.  S,  1910. 


Fig.  73. — This  Specimen  Show.s  a  Dissection  of  the  Aukiculo-ventricular  Bundle 
(Bundle  of  His)  in  the  Heart  of  a  Bullock. 
The  bundle  is  about  5  mm.  in  diameter  and  can  be  seen  grayer  than  the  rest  of  the  mus- 
culature, running  directly  up  the  middle  of  the  specimen  in  the  left  ventricle  until  it  disappears 
beneath  the  heart  muscle.  In  the  right  ventricle  it  runs  obliquely  upward  toward  the  left, 
disappearing  beneath  the  auriculo-ventricular  valve.  (Dissection  by  Dr.  Krumbhaar.)  The 
nujierficial  ponlion  of  the  bundle  and  its  'proximity  to  the  aortic  and  mitral  valves  indicate  how 
rea/lily  this  structure  might  suffer  damage  in  case  of  an  inflammatory  or  degenerative  process  in- 
volving either  of  these  valves  or  the  intervening  endocardium. 


XIII.  CONGENITAL  LESIONS 

IMPERFORATE  VENTRICULAR  SEPTUM 

An  imperforate  interventricular  septum,  like  other  congenital 
abnormalities,  is  a  condition  which  may  be  associated  with  other 
developmental  malformations — harelip,  cleft  palate,  polydactylism, 
supernumerary  auricles,  nipples,  etc.  It  is  the  commonest  of  all 
congenital  heart  lesions.  It  is  generally  associated  with  other 
defects,  such  as  obstruction  of  the  pulmonary  or  tricuspid  orifices. 
The  perforation  usually  occurs  in  the  undefended  space,  just 
beneath  the  aortic  valves.  As  a  result  of  it  hypertrophy,  and 
especially  dilatation  of  the  right  heart,  occur  if  the  child  lives  long 
enough.     Among  the  Philadelphia  Hospital  autopsies  the  following 

Fig.  74. — Patulous  Interventricular  Septum. 

C.  R.,  male,  white.  Italian  boy.  (Pennsylvania  Hospital  Autopsy  1111.  Spec.  No. 
453.     Physician:   Dr.  M.  J.  Lewis.     Pathologist:   Dr.  Krumbhaar.) 

Clinical  Notes:  Patient  admitted  unconscious,  with  left-sided  paralysis.  Has  never  had 
any  acute  illness  previously.  Was  a  "blue  baby,"  and  had  always  remained  cyanotic.  He 
did  not  play  actively.  Fingers  and  toes  are  clubbed.  For  three  days  he  had  had  fever,  head- 
ache, convulsions,  abdominal  pain.     A  loud  systolic  murmur  was  heard  over  the  heart. 

Pathologic  Diagnosis:  Congenital  malformation  of  the  heart.  Stenosis  of  the  conus 
arteriosus.  Hypoplasia  of  the  pulmonary  artery.  Patulous  interventricular  septum.  Acute 
endocarditis.     Softening  of  the  right  cerebral  hemisphere. 

Heart:  Weighs  250  gm.  Pericardium:  negative.  The  heart  is  enlarged,  especially  to 
the  right  side.  The  ductus  arteriosus  is  easily  found  and  measures  9  cm.  in  length,  2  cm.  in 
diameter.  It  does  not  admit  a  probe.  On  opening  the  heart :  at  the  junction  of  the  interauricular 
and  interventricular  septa  there  is  a  large  opening  between  the  right  and  left  sides  (undefended 
space);  it  is  about  9  cm.  in  diameter,  easily  admitting  an  ordinary  lead-pencil.  Its  walls  are 
smooth  and  lined  with  endocardium.  It  is  evidently  congenital.  Foramen  ovale  closed.  Right 
ventricle  8  mm.  Pulmonary  artery  and  the  conus  arteriosus  poorly  developed  and  stenotic. 
A  few  millimeters  below  the  base  of  the  valve  there  are  some  fine  granular  vegetations.  The 
left  ventricle  12  mm.  The  heart  muscle  is  deep  red,  normal  in  color.  The  tricuspid  valve 
measures  7  cm.  in  circumference,  the  mitral  6  cm.,  the  aorta  3.1  cm.  The  pulmonary  and 
aortic  rings  were  not  measured,  in  order  to  preserve  the  specimen.  The  coronaries  are 
normal. 

Microscopic  Examination:  The  muscle-fibers  are  swollen  and  everywhere  the  striations 
are  poorly  marked  or  absent,  the  fibers  having  a  homogeneous  appearance.  The  nuclei  are  for 
the  most  part  normal,  though  occasionally  very  large  ones  are  found.  The  papillary  muscles 
on  cross-section  show  vacuolization  of  many  fibers.  Interstitial  tissue  is  increased  in  a  few 
places.  The  endocardium  is  normal  except  for  a  slight  thickening  on  the  internal  surface  of  the 
papillary  muscle. 

206 


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208  STUDIES  IN  CARDIAC  PATHOLOGY 

lesions  of  the  interventricular  septum  were  found:  aneurism,  1; 
ulceration,  1;  rupture,  1;  perforation,  2.  (See  Figs.  74,  76,  77.) 
The  "observations  by  His  and  others  have  not  confirmed 
Rokitansky's  view  of  this  extension  upward  of  the  interventricular 
septum  to  form  the  aortic  wall,  but  show  that  the  aortic  septum 
is  prolonged  downward  to  assist  in  closing  the  interventricular 
septum  at  the  undefended  space.  Moreover,  independent  defects 
of  the  interventricular  septum,  sometimes  of  large  size  and  evi- 
dently not  of  inflammatory  origin,  and  unassociated  with  any 
deviation  to  the  right  of  the  aorta,  ma,y  and  do  occur.  Such 
conditions  cannot  be  explained  on  Rokitanskj^'s  theory  as  a 
deviation  of  the  septa,  and  must  be  acknowledged  to  be  a  primary 
arrest  of  growth  of  unknown  origin."  (Abbott.)  The  effect  of  an 
imiDcrforate  ventricular  septum  upon  the  circulation  and  upon 
the  rest  of  the  heart  dej^ends  upon  whether  it  occurs  as  an  isolated 
lesion  or  not.  In  78  per  cent,  of  Abbott's  cases  it  appeared  in 
combination  with  other  defects;  most  commonly  with  pulmonary 
stenosis.  When  it  occurs  alone,  it  produces  hypertrophy  of  both 
ventricles,  the  degree  of  which  is  dependent  upon  the  size  of  the 
perforation.  "As  the  right  ventricle  hypertrophies  and  pressure 
in  the  right  ventricle  increases,  the  leakage  diminishes,  so  that  the 
effect  of  the  lesion  tends  to  correct  itself;  on  the  other  hand,  the 
pressure  in  the  pulmonary  artery  increases.  But  since  the  ordinary 
resistance  in  the  pulmonary  circulation  is  much  less  than  in  the 
systemic,  when  the  forces  of  both  ventricles  approximate  one 
another  the  effect  on  the  pulmonarj^  circulation  is  the  same  as 
though  the  left  ventricle  became  weaker  and  the  right  remained 
unchanged.  Pulmonaiy  engorgements  may,  therefore,  result, 
with  consequent  dyspnea.  In  most  cases,  however,  the  hyper- 
trophy does  not  reach  this  point,  and  it  is  only  when  the  heart  is 
stimulated  by  effort  or  exercise  that  pulmonary  engorgement  sets 
in."     (Hirschfelder.) 


Fig.  75. — Patent  Ductus  Arteriosus. 

Male  infant,  thirty-four  days  old.  (Physician:  Dr.  G.M.Boyd.  Pathologist:  Dr.  A.  G. 
Ellis.') 

Clinical  Notes:  At  birth  the  baby  was  cyanotic  and  weighed  7  pounds.  Respiratory 
difficulty  was  present  at  all  times,  and  the  cyanosis  was  marked  during  the  first  few  days. 
Later  the  blueness  became  less  prominent,  especially  during  short  periods  in  which  it  almost 
disappeared.     Death  occurred  during  an  attack  of  dyspnea  associated  with  cyanosis. 

Pathologic  Diagnosis:  Transposilion  of  the  aorta  and  the  pulmonary  artery;  patent 
diictics  arteriosus;  hypertrophy  of  the  right  ventricle.  Patent  foramen  ovale;  partial  atelectasis 
of  the  right  lung;  general  visceral  congestion. 

Pathologic  Notes:  The  heart  is  essentially  normal  in  size.  The  wall  of  the  right  and 
left  ventricles  are  respectively  5  and  7  mm.  in  thickness.  Neither  the  pulmonary  artery  nor 
the  aorta  shows  any  evidence  of  stenosis.  The  foramen  ovale  is  patulous  in  the  form  of  a 
slit-like  opening  0.5  cm.  in  length,  and  the  ductus  arteriosus  allows  with  ease  the  passage  of  a 
probe  2  mm.  in  diameter.  Neither  the  ventricles  nor  the  auricles  are  transposed,  and  the  veins 
of  the  latter  arc  normally  placed.     (Specimen  from  the  Philadelphia  Hospital.) 

'  Case  reported  by  Dr.  A.  O.  Ellis:  Am.  Jour.  Obstet.,  1905,  lii,  No.  6. 


210  STUDIES   IN    CARDIAC    PATHOLOGY 


Fig.  76. — Patulous  Interventricular  Septum  with  Acute  Endocarditis. 

(Pennsylvania  Hospital.  Physician:  Dr.  H.  M.  Fisher.  Pathologist:  Dr.  G.  C.  Robin- 
son.) 

Clinical  Notes:  Patient  had  dyspnea  and  cough  after  exertion,  but  was  otherwise  fairly 
healthy.  Heart:  hypertrophied,  loud  systolic  murmur  at  the  apex,  transmitted  to  the  back. 
Also  a  diastolic  murmur,  loudest  over  the  aortic  area.  Two  years  later  the  patient  died  after 
ha,ving  suffered  from  gangrene  of  the  nose,  the  ear,  etc.,  apparently  the  result  of  thrombosis. 

Pathologic  Notes:  Partial  autopsy  disclosed  hydrothorax,  parenchymatous  nephritis, 
capillary  hemorrhages,  etc.,  and  the  following  cardiac  condition: 

Heart  :  Is  somewhat  enlarged ;  the  epicardium  is  normal,  but  shows  a  very  small  amount 
of  fat.  Tricuspid  valve  (after  hardening)  measures  10.5  cm.  The  wall  of  the  right 
ventricle  measures  8  to  10  mm.;  its  cavity  about  normal.  Tricuspid  valve  and  the  chordae 
tendineae  of  its  posterior  leaflet  show  a  few  fresh  vegetations.  In  the  seplum  ventriculorum, 
just  to  the  left  of  the  begiyming  of  the  conus  arteriosus,  there  is  an  oval  opening,  3.5  x  2.5  cm. 
in  diameter,  which  appears  as  a  funnel-shaped  excavation  in  the  ventricular  septum.  The  open- 
ing into  the  left  ventricle  is  nearly  closed  by  large  wart-like  vegetations.  These  vegetations  extend 
from  the  opening  upward  into  the  conus  arteriosus  and  are  continuous  with  those  on  the  right  an- 
terior leaflet  of  the  pulmonary  valve.  The  conus  arteriosus  is  quite  narrowed.  Its  origin,  which 
is  but  4.5  cm.  in  circumference,  is  surrounded  by  a  row  of  delicate  vegetations.  The  pulmonary 
artery  at  the  base  of  the  valves  measures  7  cm.  in  circumference.  All  of  its  leaflets  show  a  con- 
siderable thickening  and  puckering  and  are  the  seats  of  extensive  fresh  vegetations.  The  right 
anterior  and  posterior  leaflets  show  round  knob-like  masses  measuring  2  to  5  mm.  in  diameter, 
hanging  to  their  free  margins,  while  the  left  anterior  pulmonary  leaflet  is  about  half  covered  by 
large,  rather  regular  vegetations  extending  all  the  way  across  its  free  margin.  There  is  a  small 
group  of  warty  vegetations  extending  1.5  cm.  below  this  leaflet  in  the  conus  arteriosus,  and 
within  the  sinus  of  Valsalva  above  it  there  is  a  small  nodular  vegetation,  6  mm.  in  diameter, 
attached  to  the  wall  of  the  pulmonary  artery.  Upon  examining  the  left  side  of  the  heart  the 
auricle  is  found  to  be  normal  in  proportions.  The  mitral  valve  is  somewhat  thickened  toward  its 
base,  but  is  free  from  vegetations.  The  wall  of  the  left  ventricle  is  but  slightly  thickened  {14  mm.). 
Directly  beneath  the  posterior  leaflet  of  the  aortic  valve  there  is  an  opening  in  the  septum  ventriculorum 
continuous  with  that  seen  in  the  right  ventricle.  On  the  left  side  the  opening  measures  2.5  x  1.5  cm. 
It  is  almost  closed,  however,  by  the  extensive  vegetations  springing  from  its  margins.  The  endo- 
canliimi  of  the  left  ventricle  extends  into  the  opening  and  is  apparently  continuous  luith  that  of  the 
riijlil  rriilnrlr.  The  direction  of  the  passage  between  the  ventricles  is  downward  and  backward 
from  the  left  to  the  right  side.  The  aortic  ring  measures  6  cm.  in  circumference.  All  of  the 
aortic  valves  are  much  thickened  and  somewhat  contracted.  On  the  anterior  and  right  pos- 
terior leaflets  there  are  small  verrucose  vegetations;  on  the  left  posterior  leaflet  there  is  an  enor- 
mous, irregularly  round,  nodular  vegetation  measuring  2.5  x  2.3  x  l.S  cm.  in  diameter.  The 
vegetation  is  attached  to  the  entire  ventricular  aspect  of  the  leaflet,  and  extends  downward  into  the 
opening  in  the  septum  ventriculorum,  nearly  closing  the  same.  No  bacteriologic  examination 
was  made. 


Kjc;.  70. 


212  STUDIES    IN    CARDIAC    PATHOLOGY 

TRANSPOSITION  OF  THE  GREAT  VESSELS 

Transposition  of  the  great  vessels  is  generally  associated  with 
a  transposition  of  the  other  viscera.  It  is  ascribed  to  non-rotation 
of  the  aortic  septum  from  which  these  vessels  are  formed,  and  it 
is  often  accompanied  b}'  patency  of  the  foramen  ovale,  interven- 
tricular septum,  or  ductus  arteriosus. 

"In  typical  cases  the  aorta  is  in  front  and  to  the  right,  the  pulmonary  artery 
behind  and  to  the  left.  At  one  stage  in  the  normal  process  both  vessels  are 
connected  with  the  right  ventricle,  the  change  of  the  aorta  to  the  left  being 
largely  accomplished  by  the  completion  of  the  interventricular  septum.  Irregu- 
larities in  the  formation  of  this  septum,  especially  its  deviation  to  the  right  or 
left,  may  result  in  both  vessels  arising  from  one  or  other  of  the  ventricles,  more 
often  the  right,  an  anomaly  not  exceedingly  rare.  Transposition  of  the  vessels 
may  be  accompanied  by  transposition  of  the  auricles  and  veins,  or  of  the  ven- 
tricles, or  both.      The  transposed  vessels  may  be  normal,  but  usually  are  not."^ 

As  to  the  frequency  of  the  condition,  Theremin  found  21  cases  among  106 
cardiac  anomahes  at  the  Foundling  Hospital  in  St.  Petersburg,  and  Vierordt, 
76  among  383. 

PATULOUS  DUCTUS  ARTERIOSUS 

In  an  excellent  and  comprehensive  article  Goodman-  has  re- 
cently summarized  what  is  at  present  known  regarding  patency  of 
the  ductus  arteriosus.  Altogether  he  was  able  to  collect  71  cases, 
34  of  which  were  autopsied.  A  great  many  different  explanations 
have  been  offered  as  to  the  modus  operandi  by  which  the  ductus 
Botalli  is  normally  obliterated  during  the  first  four  weeks  of  life, 
and  an  equal  number  of  hypotheses  offered  as  to  the  cause  of  its  con- 
tinued or  renewed  patency.  Among  the  former  the  following  may 
be  mentioned:  Pressure  equilibrium  between  the  aorta  and  pulmon- 
ary artery,  also  contraction  of  the  walls  of  the  duct  after  the  first 
inspiration;  changes  in  the  position  of  the  heart  after  the  last-named 
act;  redundant  valve-like  intimal  folds  at  the  aortic  orifice,  etc. 

Persistent  patulosity  may  occur: 

1.  As  an  isolated  lesion. 

2.  In  association  with  other  cardiac  malformations. 

'  Abbott:  Osier's  Modern  Medicine,  vol.  iv,  p.  370. 

=  E.  H.  Goodman:  Univ.  of  Penna.  Med.  Bull.,  Dec.,  1910,  p.  .509.     (Complete  biljliography.) 


I-IG. 


-Patulol's  Intehventkutlak  Settum  with  Acute  Knuocahditis. 


The  interventricular  septum  is  patulous,  but  this  opening  is  almost  entirely  closed  by  a 
large  mass  of  recent  veRetations  which  are  attached  to  its  margins.  (Photograph  by  Dr.  A.  R. 
Alien.) 


214  STUDIES    IN    CARDIAC    PATHOLOGY 

3.  In  association  with  other  non-cardiac  developmental  defects. 
The  form  of  the  ductus  arteriosus  may  be  as  follows  (Gerhardt) : 

1.  Extreme  shortening  of  the  canal,  the  great  vessels  being 
practically  united  by  a  simple  opening  between  them. 

2.  A  funnel-shaped  opening,  with  the  larger  opening  on  the 
aortic  end.     (Relatively  common.) 

3.  A  cj'Iindrical  shape.     (Commonest  variety.) 

4.  Aneurismal  dilatation. 

Patency  of  the  ductus  Botalli,  both  as  an  isolated  lesion  and  in 
combination  with  other  defects,  is  one  of  the  commoner  congenital 
abnormalities.     (See  Figs.  75,  83,  84.) 

PATULOUS  FORAMEN  OVALE 

Occurrence. — A  patulous  foramen  ovale  is  a  relatively  common 
autopsy  finding  (Vierordt,  28  per  cent.;  Zahn,  22.3  per  cent.), 
but  mere  patency  is  not  necessarily  of  pathologic  importance. 
The  fact  that  the  channel  runs  obhquely  through  the  auricular 
septum,  and  that,  therefore,  the  openings  on  the  two  sides  are  not 
directh'  opposite  to  each  other,  favors  competency,  for  as  soon  as 
intra-auricular  pressure  on  the  two  sides  of  the  membranes  rises, 
the  lateral  walls  of  the  channel  are  pressed  together,  and  tend  to 
close.  Under  normal  circumstances  obliteration  of  the  opening 
is  said  to  result  from  mechanical  irritation,  as  the  result  of  which 
the  endothelial  covering  of  the  two  surfaces  becomes  abraded 
and  adhesion  follows.  The  above-mentioned  figures  apparently 
include  all  grades  of  patency.  An  opening  large  enough  to  admit 
the  small  finger  occurred  only  9  times  in  462  autopsies  (1.9  per 
cent.).^  At  the  Philadelphia  Hospital  there  were  only  recorded 
86  cases  among  8,640  autopsies  (0.9  per  cent.). 

"The  foramen  ovale  lies  in  almost  a  horizontal  plane,  and  not 
vertically  and  facing  the  left."  Neither  the  right-  nor  the  left- 
sided  posture  after  birth  is,  therefore,  of  any  consequence  in  favor- 
ing its  closure  in  the  newly  born  infant  (Fetterolf  and  Gittings).- 

1  Hintze  and  Ogle:  quoted  Hirschfelder,  "Diseases  of  the  Heart  and  Aorta,"  1910,  p.  466. 
'Fetterolf  and  Gittings:  Am.  Jour.  Children's  Dis.,  Jan.,  1910,  No.  1. 


Fig.  78. — Patulous  Foramen  Ovale. 
Hfart  of  a  woman  aged  seventy  years,  who  died  of  croupous  pneumonia,  liaving  advanced 
general  arteriosclerosis.  The  illustration  shows  a  chronic,  more  or  less  diffuse,  mitral  thicken- 
ing, with  contraction  of  the  ehorchc  tendineie,  and  marked  hypertrophy  of  the  left  ventricle. 
The  foramen  ovale  is  quite  large  and  patulous,  but  owing  to  its  oblique  course  it  was  probably 
functionally  competent. 


216  STUDIES    IN    CARDIAC    PATHOLOGY 

Pathologic  Physiology. — As  has  already  been  intimated,  mere 
patulousness  of  the  foramen  ovale  need  be  of  but  little  consequence 
unless  the  opening  be  a  very  large  and  direct  one.  (See  Figs. 
78,  79,  80.)  With  valvular  disease  of  the  heart,  especially  in 
mitral  lesions  with  failing  compensation,  the  defect  maj^  become 
important.  Thus,  for  instance,  when  the  left  auricle  is  over- 
burdened and  dilated,  and  its  internal  pressure  increased,  consider- 
able quantities  of  blood  may  regurgitate  into  the  right  auricle. 
Up  to  a  certain  point  such  reflux  may  be  conservative,  after  the 
manner  of  the  safety-valve.  When  the  failure  of  the  right  heart 
is  superadded,  however,  a  patulous  foramen  ovale  becomes  doubly 
disadvantageous  by  preventing  proper  aeration  of  the  blood,  and 
by  directly  mixing  the  venous  with  the  arterial  currents.  Griffiths 
suggests  that  slight  patency  of  the  foramen  may  be  of  actual 
benefit  in  case  of  obstruction  in  the  pulmonary  circulation,  such 
as  emphysema,  since  it  is  less  harmful  to  have  some  venous  blood 
admitted  to  the  arteries,  than  to  have  the  individual  waterlogged 
from  back-pressure  in  the  right  heart.  Emboli  from  the  right 
heart  may  reach  the  general  circulation  by  passing  through  a 
patulous  foramen  ovale  or  interventricular  septum  or  ductus 
arteriosus. 

ABNORMAL  FIBROUS  BANDS 

The  so-called  abnormal  fibrous  bands  of  the  heart  are  chiefly 
found  in  the  ventricles.  According  to  Tawara,  they  represent 
a  congenital  anomaly  of  the  auriculo-ventricular  bundle;  an 
opinion  based  solely  on  their  course  and  distribution.  Roessle^ 
showed  that  these  fibrous  bands  contained  muscular  tissue,  but 
regarded  their  structure  as  the  result  of  pressure  atrophy.  Magnus- 
Alsleben-  examined  ten  cases  and  found  muscle-cells  often  similar 
in  microscopic  appearance  to  the  auriculo-ventricular  bundle.  He 
suggests  that,  inasmuch  as  these  bands  are  of  no  such  great  rarity, 
both  the  hitherto  employed  terms  "  abnormale  "  and  "  sehnenfaden  " 
are  inappropriate.     (See  Fig.  82.) 

'  Roessle:  Arch.  f.  klin.  Med.,  1902,  p.  224. 

2  Magnus-Alsleben:  Centralb.  f.  Path.  u.  path.  Anat.,  1906,  p.  897. 


Fig.  79. — Patulous  but  Competent  Foramen  Ovale.     (University  of  Pennsylvania 
Museum.) 


Fig.  so. — P.\tulous  but  Inxompetent  For.v.mex  0\  ale.     (Pennsylvania  Hospital,  Xo.  175. 


CONGENITAL    LESIONS  219 

ANOMALIES  OF  THE  SEMILUNAR  VALVES 

These  anomalies  may  occur  in  otherwise  normal  hearts  and 
have  little  clinical  significance,  or  they  may  be  associated  with 
coarction  of  the  aorta.  Theremin  has  reported  an  instance  in 
which  both  the  aortic  and  pulmonic  valves  were  bicuspid.  There 
has  been  considerable  discussion  as  to  whether  the  condition  was 
most  frequently  the  result  of  faulty  development  or  of  antenatal 
endocarditis.  Fusion  of  the  leaflets  resulting  from  post-natal 
infections  "is  distinguished  by  the  presence  behind  the  fused 
cusps  of  a  high  raphe  formed  by  their  united  adjacent  portions, 
by  the  absence  of  compensatory  changes  in  this  and  in  the  fused 
cusp,  and  by  marked  thickening,  calcification,  and  other  evidence 
of  inflammator}''  action"  (Abbott). 

This  anomaly  may  be  attended  by  no  pathologic  results,  but 
not  infrequently  acute  endocarditis,  arteriosclerotic  change,  or 
functional  insufficiency  as  the  result  of  valvular  stretching  is  a 
sequel  of  this  condition. ^     (See  Figs.  81,  82,  83.) 

DOUBLE  MITRAL-  OR  TRICUSPID'  ORIFICES 

Double  orifices  have  been  reported.  The  abnormal  orifice 
may  possess  its  own  papillarj^  muscles  and  chordse  tendinese. 
"Pisenti  explained  the  condition  as  the  result  of  a  congenital 
fenestration  which  had  transmitted  the  blood-stream  in  early 
embryonic  life,  and  thought  that  its  transformation  into  a  second 
valvular  orifice  was  an  adaptation  of  growth  or  compensatory 
process,  the  papillary  muscles  (which  develop  at  the  same  time  as 
the  cusps)  growing  up  with  their  chordae  tendinese  to  its  borders." 
f Abbott.)  This  hypothesis  is  tentatively  indorsed  by  the  last- 
named  authoress,  although  rejected  by  Cohn  on  the  ground  that 
the  anomaly  docs  not  correspond  with  what  we  know  regarding 
any  stage  of  the  embryologic  process.     (See  Fig.  85.) 

'  For  literature  .sec:  Dilg,  Virchow's  Archiv.,  1883,  vol.  xci;  Lannois  and  Villaret,  Bull, 
et  Mom.  Soc.  Anat.,  Pari.s,  July,  190.5. 

^  (jrtMnfuM:  Tran.s.  Path.  Hot;.  U)n(lon,  1876,  xxvii,  p.  128.  Colin:  Inauuuial  Di.s.sei-l. 
Konig.'ibcrg,  1800.    Abbott:  0«ler's  ".VIotU'rn  .Medicine,"  vol.  iv,  p.  393. 

'  PiHenti:  "  Di  una  variwHirna  .\nonialia  della  triouspido,"  Peiinia,  1888. 


-Bicuspid  Pulmonary  Valve.     (Specimen  from  the  Mutter  Museum  of  the  College 
of  Physicians  of  Philadelphia.) 


Fig.  82. — Four  Pulmonary  Valves.     (Specimen  from  the  Philadelphia  Hospital.) 

This  anomaly  is  somewhat  more  frequent  in  the  pulmonary  artery  than  in  the  aorta.  It 
usually  has  no  pathologic  significance,  but  congenitally  abnormal  valves  seem  to  be  more 
frequently  subject  to  subsequent  infection. 


222  STUDIES  IN  CARDIAC  PATHOLOGY 


Fig.  83. — Congenital  Atresia  of  the  Aorta,  with  Patent  Ductus  Arteriosus. 

Male,  negro,  aged  twenty-two  years.  (W.  B.)  (Pennsylvania  Hospital,  1903.  No. 
1711.     Autopsy  472.) 

Clinical  History:   Pneumonia  as  a  boy;  and  again  1898.     Gonorrhea  some  years  ago. 

Symptoms:   dyspnea,  tachycardia,  arrhythmia. 

Apex-beat  in  fifth  interspace,  mid-clavicular  line,  heart  enlarged  to  the  right.  First 
sound  booming.  No  murmurs  on  admission,  but  later  a  soft  systolic  murmur  was  heard  at  the 
apex  from  time  to  time,  but  not  constantly. 

Pathologic  Diagnosis:  Congenital  atresia  of  the  aorta,  mth  patent  ductus  arteriosus. 
Bicuspid  aortic  valve.  Chronic  mitral  endocarditis.  Cardiac  hypertrophy,  especially  of  the 
right  side.  Thrombosis  of  the  right  innominate,  internal  jugular,  axillary,  and  basilic  veins; 
also  of  the  auricular  appendage.     Congestion  of  the  viscera,  with  cardiac  hepatic  cirrhosis,  etc. 

Pericardium  and  Heart,  very  large,  filling  the  whole  anterior  mediastinum.  Heart 
extends  8  cm.  to  right  of  mid-sternum,  at  level  of  fourth  costal  cartilage.  From  above  down- 
ward it  measures  13  cm.;  from  the  apex  diagonally  to  the  base,  20  cm.  Pericardium  contains 
400  c.c.  shghtly  turbid,  straw-colored  fluid,  containing  a  few  flakes  of  fibrin.  The  serous  sur- 
faces are  smooth  and  glistening.  Heart  weighs  780  gm.  It  is  large  and  has  a  peculiar  square 
shape,  the  apex  being  very  blunt.  The  right  heart  is  especially  large.  The  epicardium  in  some 
places  appears  thickened,  and  is  rather  opaque  and  grayish.  Subepicardial  fat  decreased. 
The  vessels  are  much  injected  and  small  punctate  hemorrhages  are  seen,  especially  at  the  base. 
The  cavities  are  all  filled  with  postmortem  clots.  Both  the  right  auricle  and  ventricle  are 
large  and  their  walls  excessively  thickened.  The  tricuspid  orifice  measures  12  cm.  in  circum- 
ference; its  valves  are  thin  and  delicate.  Pulmonary  orifice  9  cm.  in  circumference.  Papillary 
muscles  and  columnee  carnese  are  exceedingly  large  and  firm.  The  actual  wall  of  the  right 
ventricle  measures  10  to  IT  mm.  in  thickness,  it  being  as  thick  as  a  moderately  hypertrophied  left 
ventricle.  Wall  of  the  right  auricle  3  to  8  mm.  The  tip  of  the  auricle  is  completely  filled  with 
a  soft,  gray,  smooth  thrombus,  the  center  of  which  contains  a  thick,  gray,  pus-like  material. 
Mitral  valves  thin  and  delicate.  The  aortic  valve  shows  only  two  large  cusps,  hut  they  are 
thin  and  delicate.  The  aortic  orifice  is  5.5  cm.  in  circumference  (half  the  size  of  the  pulmonary) ; 
the  aorta  above  it  is  about  the  same  size.  The  cavity  of  the  left  ventricle  is  not  very  large,  but  the 
walls  are  much  hypertrophied,  averaging  18  to  20  mm,,  in  thickness.  The  endocardium  is  opaque, 
thick,  and  white.  Muscular  bands  extend  from  one  side  of  the  wall  to  the  other,  forming  a  coarse 
network  in  the  cavity.  Coronary  arteries  are  large  and  patent.  A  few  pinhead-sized,  raised 
points  are  scattered  over  the  aorta. 

Microscopic  Diagnosis:  Chronic  interstitial  myocarditis.  Pericardium  shows  no  especial 
change.  Heart  muscle  shows  degenerative  changes  in  places,  while  a  fibrillated  connective 
tissue  containing  very  few  cells  fills  the  areas  of  degeneration  and  extends  between  the  muscle- 
fibers,  the  latter  being  large  and  granular.  Endocardium  is  thickened;  connective  tissue  ex- 
tends from  it  to  the  muscle.     (Aorta  shown  in  Fig.  84.) 


l''ifi.  S?>. — Hicrsrin  Aortic  Valve. 

This   hpocinioM   also   .shows   marked   left   ventricular   hypertrophy  and    "abnoniKd  fibrous 
bands"  traversing  this  chamber.     (See  p.  222.) 


Fic.  84. — Congenital  Aortic  Stenosis  with   Patency  of  the  Ductus  Arteriosus. 

Pathologic  Notes:  The  aorta  is  very  small,  measuring  at  the  arch  only  4.5  cm.  in  di- 
ameter, while  the  pulmonary  artery  is  twice  this  size.  The  innominate,  left  vertebral,  and  sub- 
(•l:i\ian  urlcrifs  are  normal  in  position  and  size.  Immeiialdy  at  the  junction  of  the  lower  edge  of 
Ihi:  li-fl  .inhrliii'ian  artery  and  the  aorta,  the  latter  vessel  shows  a  sudden  and  marked  constriction, 
ll.e  external  diameter  of  which  measures  12  mm.,  while  S  cm,,  above  and  below  the  constriction  the 
aorta  mcanureH  2  and  2.5  cm.  in  diameter.  On  opening  the  aorta  and  looking  down  toward  the 
fonstriction  the  ves-iel  appears  to  end  in  a  smooth,  rounded,  blind  pouch,  but  on  closer  in- 
spection a  fjinhoad-sissed  opening  can  bo  seen,  through  which  a  small  probe  can  be  passed. 
Connecting  the  pulmonary  artery  just  where  it  branches,  and  the  aorta  just  at  the  proximal 
side  of  the  constriction,  is  a  narrow  ve.s.sel,  about  S  mm.  in  length  and  .5  mm.  in  diameter, 
through  which  a  [jrobc  can  be  passer!..  The  aorta  throughout  its  length  is  narrow,  but  its 
branches  are  about  normal  in  size.  (■Pennsylvania  Hospital,  Xo.  .S17.  Thae  are  the  vessels 
belonging  to  the  heart  nhown  in  Fi;i.  HS.) 
13 


226  STUDIES  IN  CARDIAC  PATHOLOGY 


Fig.  85. — Double  Mitral  Orifice. 

C.  D.,  male,  aged  twenty-two  years.     (Pennsylvania  Hospital  23.5.     349.) 

Clinical  Notes:  Patient  died  of  typhoid  fever,  complicated  by  bronchopneumonia  and 
erysipelas.  He  had  had  no  circulatory  symptoms  at  any  time  before,  nor  physical  signs  in- 
dicative of  cardiac  disease. 

Pathologic  Notes:  Heart  weighs  290  gm.  The  cavities  are  normal  in  proportion, 
except  the  left  auricle,  which  is  dilated.  All  of  the  valves  are  normal  except  the  mitral,  which 
shows  thickening.  The  chorda;  tendineoe  are  thickened,  white,  and  fibrous.  The  papillary  muscles 
are  large  and  thick;  and  beneath  their  posterior  segment  the  three  portions  are  distinct  as  three 
separate  muscles.  The  chiinhi  IcmlitKiv  micli  from  two  of  them  to  the  anterior  leaflet,  which  is 
large,  measuring  3  cm.  from  I  In'  iiiiinihi.-i  liliriKitiK  In  I  he  free  edge  in  a  straight  line.  The  papillary 
muscle,  which  is  normally  alUivhnl  In  Ihc  rilgr  nf  lln-  vnlve,  attaches  here  almost  at  the  central  portion 
of  the  leaflet.  The  valve  is  perforated  by  an  opening  1  cm.  in  diameter,  the  chordce  tendineoe  at- 
taching about  the  margin  of  this  opening.  There  are  thus  two  auriculo-ventricular  openings,  sur- 
rounded by  chordae  tendineoe,  with  normal  margins.  The  entire  ventriculo-ventricular  ring  measures 
9.5  cm.  in  circumference.  The  heart  muscle  is  dark  reddish-brown  and  firm.  Left  ventricle: 
18  to  20  mm.  Coronaries  patent.  Foramen  ovale  closed.  Auricular  appendages  free  from 
thrombi.     Aorta  smooth. 

Microscopically:  Slight  edema  of  the  heart  muscle  with  pigmentation  of  the  muscle-fibers, 
but  no  other  changes. 

(The  match-stick  passes  through  the  accessory  auriculo-ventricular  orifice.) 


INDEX  OF  ILLUSTRATIONS 


Aneurism  of  mitral  valve,  45 
of  the  heart,  171,  173 

of  the  left  ventricle,  with  calcification,  183 
Aortic   and    mitral   endocarditis,    acute,    19, 
25,  33,  41 
chronic,  69 
endocarditis,  acute,  9,  15,  37 

subacute,  11 
mitral    and    tricuspid    endocarditis,    acute 
and  chronic,  93 
obstruction,  79 
obstruction,  61,  65 
Atresia  of  the  aorta,  224 
Auriculo-ventricular  bundle,  205 


Ball  thrombus  of  the  left  auricle,  185 
Bicuspid  aortic  valve,  223 
pulmonary  valve,  220 


Calcification  and  dilation  of  the  aorta,  163 

of  the  aorta,  161,  165,  167 

of  the  coronary  arteries,  169 
Cardiac  aneurism  and  thrombosis,  177,  181 

hypertrophy,  145 


Dilatation  of  the  heart,  159 


Endocarditis,  acute  and  chronic,  35 
chronic,  57 


Gumma  of  the  heart,  191,  193,  195 
of  the  left  ventricle,  197 


Hemopericardium,  131 

Hypertrophy  and  dilatation  of  the  heart,  139 
of  the  left  ventricle,  153,  155,  157 


Mitral  and  aortic  endocarditis,  acute,  5 
and  mural  endocarditis,  acute,  7 


Mitral  endocarditis,  acute  and  chronic,  89 
ulcerative,  3 
chronic,  91 
insufficiency,  83 
obstruction  from  the  auricular  aspect,  73 

from  the  ventricular  aspect,  53 
orifice,  double,  226 
Mural  and  aortic  endocarditis,  chronic,  59 
endocarditis,  acute,  29 
thrombosis,  179 


Patulous  ductus  arteriosus,  209 

foramen  ovale,  215,  217,  219 

interventricular  septum,  207 

with  acute  endocarditis,  211,  213 
Pericarditis,  acute  fibrinopurulent,  101 
serofibrinous,  109,  125 

chronic  adhesive.  111,  115,  119,  121 

fibrinous,  107 

subacute  fibrinous,  103 

tuberculous,  127,  129 

QuADRicuspiD  pulmonary  valve,  221 

Rupture  of  the  aorta,  133,  189 

Syphilitic  aortitis,  201,  203 

Thorax,  sagittal  section  (No.  1),  147 
(No.  2),  149 
(No.  3),  151 
transverse  section  (No.  1),  141 
(No.  2),  143 
Thrombosis  of  the  heart,  175 
Tricuspid  and  mitral  endocarditis,  chronic,  47 
obstruction,  75 

Vertical  .section  of  the  thorax,  anterior  half, 
141 
posterior  lialf,  143 


INDEX  OF  SUBJECTS 


Actinomycosis  of  the  pericardium,  118 
Aneurism  of  the  heart,  ISS 
Angina  pectoris,  186 

Anomalies  of  the  auriculo-ventricular  valves, 
218 
of  the  semilunar  valves,  218 
Aorta,  arteriosclerosis  of,  186 
coarction  of,  51 
rupture  of,  198 
syphihs  of,  168,  186,  202 
Aortic  disease  due  to  rheumatic  fever,  50 
in  locomotor  ataxia,  62 
in  syphilis,  62 
spirocheta  paUida  in,  62 
Wassermann  reaction  in,  62 
insufficiency,  55 

clinical  considerations,  63 
functional,  62 

occurrence  and  pathologic  anatomy,  55 
pathologic  physiology,  60 
obstruction,  clinical  considerations,  54 
occurrence  and  pathogenesis,  50 
pathologic  anatomy  of,  51 
physiology,  52 
orifice,  diseases  of,  50 
valve,  embryologic  formation,  56 
Aortitis,  syphilitic.  168,  186,  202.     See  also 

Diseases  of  the  A  ortic  Orifice 
Auricular  thrombosis,  8,  185 
Auriculo-ventricular  bundle,  142 

B.^cTERioLoov  of  acute  endocarditis,  12,  13, 
26 
of  pericarditis,  106,  116 

Chemical  changes  of  mj'ocardium  in  cardiac 

hypertrophy,  158 
Congenital  heart  Icsion.s,  206 
Cor  bovi.s  in  aortic  disease,  60 
Coronary  arterie.s,  180 

effects  of  obliteration,  180 

experimental  ligation  of,  182 
arteriosclero.si.H,  180 

frequency  of,  184 

pathogcneMlH,  182 


DiSE.\SES  of  the  aortic  orifice,  experimental, 
58 
unusual  cases  of,  58 

Embolism  in  acute  endocarditis,  10 

in  endocarditis,  27 
Endocardial  lesions,  statistics,  46 
Endocarditis,  acute,  1 

age  of  occurrence,  12 

auricular  thrombosis  in,  S,  185 

bacteriology,  12,  13,  26 

classification,  4 

clinical  considerations,  27 

diagnosis,  30 

embolism  in,  10,  27 

etiology,  1 

gonococcus,  21 

in  chorea,  20 

in  congenital  lesions,  211,  213 

in  malaria,  24 

in  pneumonia,  17 

in  tuberculosis,  22 

in  typhoid  fever,  24 

infarction  in,  8 

malignant,  8,  13 

morbid  anatomy,  6 

pathogenesis,  12 

pneumococcus,  20 

predisposition,  10 

rheumatic,  12,  14 

simple,  8,  13 

verrucose,  2 
bacteriology  of,  30 
chronic,  39 

clinical  considerations,  44 

duration  of  life  in,  44 

frequency  of,  43 

heredity  of,  46 

infective,  30 

bacteriology  of,  .30 
classification,  31 

morphologic  classification,  42 

post-inort(!m  frequency,  46 
in  domestic  animals,  154 
pni'umococcus,  13 


!3I 


232 


INDEX    OF    SUBJECTS 


Endocarditis,  subacute,  24 

syphilitic,  32 

trauma  as  a  cause,  34 
Experimental  myocarditis,  168 

production  of  pericarditis,  104 

valvular  lesions,  36,  58,  84,  77,  94 

Fibrous  hands  in  heart,  216 

Heart,  congenital  lesions,  anomalies  of  semi- 
lunar valves,  218 
fibrous  bands,  216 

imperforate  ventricular  septum,  206 
of  the  auriculo-ventricular  valves,  218 
patulous  ductus  arteriosus,  212 

foramen  ovale,  214 
transposition  of  the  vessels,  212 
dilatation  of,  162 

clinical  considerations,  166 
in  rheumatic  fever,  170 
pathogenesis,  162 
pathologic  anatomy,  164 
displacement  of  other  organs,  146 
foreign  bodies  in,  58,  60 
hypertrophy,    auriculo-ventricular    bundle 
in,  142 
chemistry  of,  158 
■  classification,  138 
congenital,  156 
from  beer  drinking,  154 
idiopathic,  156 
in  nephritis,  148 
in  rheumatic  fever,  170 
in  valvular  disease,  152 
Mtiller's  method  of  estimating,  158 
occurrence  of,  137 
pathogenesis,  140 
normal  dimensions  of,  136 
position  of,  in  pericardial  effusion,  123 
rupture  of,  194 

frequency,  196 
syphilis  of,  200 
thrombosis  of,  192 
tumors  of,  19S 
Hemopericardium,  110 
Heredity  and  valvular  disease,  46 
Hydrothorax  in  valvular  disease,  85 
Hypertrophy     of     the     heart.     See     Heart, 
hypertrophy  of 

Left  auricle,  dilatation  of,  70 

size  of,  68 
Liver  in  tricuspid  insufficiency,  94 


Mitral  insufficiency,  80 

experimental,  84 
frequency  of,  80 

pathogenesis,  80 

pathologic  anatomy  of,  81 
physiology,  82 
leaflets,  anterior,  function  of,  64 
obstruction,  64 

anatomy  of,  pathologic,  66 

and  congenital  malformations,  78 

and  pulmonary  tuberculosis,  68 

classification,  64 

clinical  considerations,  77 

congenital,  67 

etiology  of,  71 

experimental,  77 

functional,  64 

in  nephritis,  71 

occurrence  and  frequency  of,  71 

operative  possibilities,  77 

pathologic  physiology,  74 

thrombosis  in,  74,  194 

varieties,  64 

vocal  paralysis  in,  70 
orifice,  button-hole,  67 

diseases  of,  64 

double,  218 

embryology,  68 

funnel-shaped,  66 

size  of,  64 
sphincter,  86 

valve,  test  of,  efficiency  of,  81 
Myocardial  lesions,  statistics,  48 
Myocarditis,  acute,  166 
chronic,  168 

clinical  considerations,  176 
experimental,  168 
in  infections,  174 
rheumatic,  170 
suppurative,  174 
toxic,  174 
Myocardium,  syphilis  of,  200 

Nephritis,  in  mitral  obstruction,  71 

Papillary  muscles,  rupture  of,  196 
Patulous  ductus  arteriosus,  212 

interventricular  septum,  206 
Pericardial  effusion,  position  of  heart  in,  123 

"milk  spots,"  117 

pseudo-cirrhosis  of  liver,  124 
Pericarditis,  acute,  as  a  terminal  infection,  116 
bacteriology  of,  106 


INDEX    OF    SUBJECTS 


233 


Pericarditis,  acute,  chemistry  of,  104 

classification  and  frequency,  105 

in  gonorrhea,  117 

in  nephritis,  116 

in  pneumonia,  112 

in  sypliihs,  117 

occurrence  and  frequency,  100 

pathogenesis,  lOS 

pathologic  anatomy,  100 
physiology,  120 

statistics,  108 

toxic,  116 

trauma  as  cause  of,  104 

tuberculous,  113 
chronic,  124 

calcification  in,  128 

frequency  of,  132 

pathogenesis,  124 

pathologic  physiology,  130 

varieties  of,  126 
chnical  considerations,  134 
in  rheumatic  fever,  110 
maculae  albidse,  117 
mediastinitis  in,  124 
suppurative,  105 
Pericardium,  anthracosis  of,  110 
calcification  of,  118 
congenital  defects  of,  134 
lymphatic  circulation  of,  106 
normal  capacity,  104 
Pick's  disease,  124 
Pulmonary  artery,  disease  of,  99 
insufficiency,  98 

pathogenesis,  98 

pathologic  anatomy,  99 

relative,  functional,  98 
obstruction,  and  pulmonary  tuberculosis,  97 

pathogenesis,  96 

pathologic  anatomy,  97 
physiology,  97 
orifice,    anatomic    and     physiologic     pecu- 
liarities, 96 

diseases  of,  96 


Rheumatic  fever,  as  cause  of  acute  endocar- 
ditis, 12,  14 
of  mitral  obstruction,  71 
pericarditis  in,  110 

Stromrinne,  66 

Syphihs  and  angina  pectoris,  186 
aortitis  in,  202 
as  cause  of  aortic  disease,  62 
of  the  aorta,  168,  184 
of  the  heart,  200 
frequency,  200 
pathologic  anatomy,  200 
Syphilitic  aortitis,  168,  186,  202 

Thrombosis  in  mitral  disease,  74 
stenosis,  194 
of  the  heart,  192 
Transposition  of  the  great  vessels,  212 
Trauma  as  a  cause  of  endocarditis,  34 

of  pericarditis,  104,  108 
Tricuspid    insufficiency,     clinical    considera- 
tions, 95 
experimental,  94 
fiver  in,  94 
pathologic  anatomy,  92 

physiology,  94 
relative,  95 
lesions,  frequency  of,  86 

pathogenesis,  86 
obstruction,  congenital,  87,  90 
frequency,  87 
pathologic  anatomy,  88 
physiology,  92 
orifice,  diseases  of,  86 
Tuberculosis,    pulmonary,   effect   of   valvular 
lesions  upon,  68 

Valvular  aneurism,  43 

lesions,  experimental,  36,  58,  77,  84,  99 

hydrothorax  in,  85 

of  the  right  heart,  86 
Vocal  paralysis  in  mitral  obstruction,  70 


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